bluuebunny/crossref_metadata_2025_split huggingface dataset:
Mood, eating behaviour and attention
Authors: WILLIAMS J. M. G. , HEALY H. , EADE J. , WINDLE G. , COWEN P. J. , GREEN M. W. , DURLACH P. 
Published: October 2002

Background. Obesity is a growing health problem, but most people find dieting unsuccessful. Three studies examine possible reasons for the difficulty and the extent to which dieting-related reductions in cognitive function are associated with mood and well-being.Method. In Study One, 49 female dieters were compared with a control group of 31 matched non-dieters on measures of well-being, mood, eating behaviour (Dutch Eating Behaviour Questionnaire), and attention. Study Two examined two measures of restraint to examine why previous studies find high restrainers are prone to react to emotion. Study Three experimentally manipulated mood using music and the standard Velten Induction Procedure to examine attention in restrainers and emotional eaters.Results. Dieting was found to be associated with deficits in sustained attention. This finding was further supported by the demonstration of a significant impairment in performance following a negative mood induction in high emotional eaters whereas high restrainers were relatively unaffected by the mood challenge.Conclusions. We suggest that different aspects of eating behaviour have dissociable effects on cognitive-affective function. Trait tendencies to restrained eating are associated with attentional deficits, but are not further affected by mood disruption. It is the long-term tendency to eat when emotional that combines with current emotional state to trigger cognitive deficits.
Visuospatial memory and learning in first-episode schizophreniform psychosis and established schizophrenia: a functional correlate of hippocampal pathology?
Authors: WOOD S. J. , PROFFITT T. , MAHONY K. , SMITH D. J. , BUCHANAN J.-A. , BREWER W. , STUART G. W. , VELAKOULIS D. , McGORRY P. D. , PANTELIS C. 
Published: October 2002

Background. Despite a number of studies that have indicated impaired memory function in patients with schizophrenia, there have been few that have used a sensitive measure of right medial temporal lobe pathology. Given the reported findings of reduced hippocampal volume in schizophrenia, we used a theoretically sensitive test of the right medial temporal lobe to determine the nature of the visuospatial memory deficit in the disorder.Methods. Seventy-six patients (37 with a first-episode schizophreniform psychosis, and 39 with established schizophrenia) were compared with 41 comparison subjects on a number of tests of visuospatial memory. These included spatial working memory, spatial and pattern recognition memory and a pattern-location associative learning test.Results. Both patient groups displayed recognition memory deficits when compared to the comparison group. However, only those patients with established schizophrenia (of 9 years duration on average) were impaired on the associative learning test.Conclusions. The results indicate either a progressive decline in visuospatial associative learning ability over the course of the disorder, or that poor visuospatial associative learning is a marker for poor prognosis. In addition, these results have implications for our understanding of the role of the right medial temporal lobe in the pathophysiology of schizophrenia.
Long-term adjustment in burn victims: a matched-control study
Authors: ALTIER N. , MALENFANT A. , FORGET R. , CHOINIÈRE M. 
Published: October 2002

Background. To date, there is little information about how severely burned patients compare to unburned healthy individuals in terms of psychological profile and quality of life. As part of a larger study on the sensory consequences of burns, we assessed psychological functioning and quality of life in burned patients and unburned healthy control subjects. We also examined whether burn patients experiencing pain and/or paresthetic sensations (i.e. symptomatic patients) present a profile that is different from those who are asymptomatic.Methods. Forty-nine burned patients (% total body surface area = 34·59%±13·40; 82% males/18% females) were evaluated 63·59±28·1 months post-burn. They were matched with 49 unburned healthy volunteers on age, sex, and education level. All subjects were administered the Symptom Checklist 90-Revised (SCL-90-R) to assess psychological functioning and the 36-item Short-Form Health Survey (SF-36) to assess quality of life.Results. Approximately 25% of the burn patients presented clinically-significant psychological disturbances compared to 12% in the control group. Burn patients enjoyed a quality of life comparable to that of the control subjects, although they perceived some deterioration in their general health. More symptomatic than asymptomatic patients suffered from clinically-relevant somatization and obsessive–compulsive disturbances.Conclusions. Severely burned patients adjust relatively well, although some develop clinically-significant psychological disturbances such as somatization and phobic anxiety. Burn patients experiencing abnormal sensations in their healed wounds (i.e. symptomatic patients) do not suffer from maladjustment to a greater extent than their asymptomatic counterparts, although more symptomatic patients experience somatization and obsessive–compulsive behaviours.
Understanding cross-national differences in depression prevalence
Authors: SIMON G. E. , GOLDBERG D. P. , VON KORFF M. , ÜSTÜN T. B. 
Published: October 2002

Background. Previous epidemiological studies indicate large cross-national differences in prevalence of depression.Methods. At 15 centres in 14 countries, 25916 primary care patients were screened for common mental disorders. A stratified random sample of 5447 primary care patients completed a baseline diagnostic assessment and 3197 completed a 12-month follow-up assessment. Psychiatric symptoms and diagnoses were assessed using the Composite International Diagnostic Interview (CIDI). Interviewer-rated disability was assessed using the Social Disability Schedule (SDS).Results. Prevalence of current major depression varied 15-fold across centres. When centres were divided into three groups according to prevalence rates, the symptom pattern or latent structure of depressive illness was generally similar at low-, medium-, and high-prevalence centres. Depression was universally associated with disability, but this association varied significantly (t = 3·51, P = 0·0005) across centres. At higher-prevalence centres, depression was associated with lower levels of impairment. At 1 year follow-up, higher prevalence centres had both significantly higher rates of depression onset (t = 3·11, P = 0·002) and higher rates of persistence among those depressed at baseline (t = 2·49, P = 0·013).Conclusions. Large cross-national variations in depression prevalence cannot be attributed to ‘category fallacy’ (cross-national differences in the nature or validity of depressive disorder). Use of identical measures and diagnostic criteria may actually identify different levels of depression severity in different countries or cultures. Cross-national differences in the onset and outcome of depression may reflect either true prevalence differences or differences in diagnostic threshold.
Outcome 3 years after a road traffic accident
Authors: MAYOU RICHARD , BRYANT BRIDGET 
Published: October 2002

Background. Road traffic accidents are known to have significant consequences for mental state and quality of life in the ensuing year that are largely unrelated to the nature of the injuries. Little is known of longer-term outcome in a representative population.Methods. Questionnaires covering mental state and social adjustment were sent to 770 subjects who had previously participated in a prospective study of consecutive attenders at an emergency department following a road traffic accident and who had completed questionnaires at baseline, 3 months and 1 year. Outcomes were not predicted by measures related to injury type or severity but were predicted by baseline and later non-injury variables.Results. Replies were received from 507 (66%) subjects. Although 76% of injuries were medically minor bruises and lacerations, 132 (26%) reported symptoms of psychiatric disorder and 104 (21%) moderate or severe pain at 3 years. There was little evidence of improvement in prevalence between 1 and 3 years, with continuing physical symptoms, psychiatric disorder and reported consequences for everyday life. There was a significant reduction in the number of cases of post-traumatic stress disorder (PTSD) despite there being 21 late onset cases. Psychiatric outcomes and pain were unrelated to the severity of injury and were largely predicted by post-accident variables.Conclusions. Road traffic accidents have much greater consequences than would be expected from the largely minor nature of the physical injuries. There is a need for changes in medical care and in socio-legal procedures.
Further studies to quantify the dose of natural aerosols of foot-and-mouth disease virus for pigs
Authors: ALEXANDERSEN S. , DONALDSON A. I. 
Published: October 2002

Foot-and-mouth disease virus (FMDV) can be spread by a variety of mechanisms, including wind. Simulation models, developed to predict the risk of airborne spread, have played an important part in decision making in some outbreaks. The amount of airborne virus excreted as well as the minimal infectious dose (MID) of FMDV for different species are important determinants of airborne spread. The objective of this study was to obtain data for the O1 Lausanne, O SKR 2000 and O UKG 2001 strains of FMDV to enhance the capability of such models. Pigs were exposed to naturally generated aerosols of the three strains using an experimental design which delivered high doses of the two strains O1 Lausanne and O SKR 2000 over a short period, or of the O UKG 2001 strain over an extended period. The average excretion of the O1 Lausanne strain was 106·4 TCID50 per pig per hour. The excretion of the O SKR 2000 strain averaged 105·8 and the O UKG 2001 strain 106·1 TCID per pig per 24 h. The results show that the previous estimate of ‘above’ 800 TCID50 as the MID50 for the O1 Lausanne strain is a considerable under-estimate and that the real dose may be as high as 6000 TCID50. A dose of around 650 TCID50 of the O SKR 2000 strain failed to infect any pigs. Thus, the aerosol MID50 for pigs for this isolate is at least 1000 TCID50 and likely to be as high or higher than the O1 Lausanne strain. The exposure of pairs of recipient pigs kept physically separated from donor pigs in a series of rooms to aerosol exposure doses of the O UKG 2001 strain of around 50 TCID50 per min for 24–48 h failed to infect any of eight pigs. Thus, the present experiment confirms our previous findings [1, 2] that pigs, compared to cattle and sheep, are relatively resistant to infection with airborne FMDV.
Molecular mechanisms of sulfasalazine‐induced T‐cell apoptosis
Authors: Liptay Susanne , Fulda Simone , Schanbacher Marta , Bourteele Soizic , Ferri Karine F , Kroemer Guido , Adler Guido , Debatin Klaus M , Schmid Roland M 
Published: October 2002

Impaired apoptosis of T‐lymphocytes is involved in the development of chronic inflammatory disorders. Previously we have shown that the anti‐inflammatory drug sulfasalazine induces apoptosis in a murine T‐lymphocyte cell line. The aims of the present study were to expand these observations to human systems and to analyse the molecular basis for sulfasalazine‐induced apoptosis.
Sulfasalazine induces apoptosis both in Jurkat cells, a human T‐leukaemia cell line (ED50 value ∼1.0 mM), and in primary human peripheral blood T‐lymphocytes (ED50 value ∼0.5 mM). In contrast SW620 colon carcinoma cells or primary human synoviocytes are not affected at these concentrations suggesting a cell type‐specific sensitivity to sulfasalazine.
Sulfasalazine triggers the mitochondrial accumulation of Bax and induces a collapse of the mitochondrial transmembrane potential (ΔΨm).
Sulfasalazine causes cytochrome c release from mitochondria and subsequent activation of caspase‐3 and downstream substrates. However, the pan‐caspase inhibitor Z‐VAD.fmk fails to inhibit sulfasalazine‐induced apoptosis.
Sulfasalazine stimulates mitochondrio‐nuclear translocation of the novel apoptogenic factor apoptosis‐inducing factor (AIF) and triggers large‐scale DNA fragmentation, a characteristic feature of AIF‐mediated apoptosis.
Sulfasalazine‐induced ΔΨm loss, AIF redistribution, and cell death are fully prevented by overexpression of Bcl‐2.
In conclusion, our data suggest that sulfasalazine‐induced apoptosis of T‐lymphocytes is mediated by mitochondrio‐nuclear translocation of AIF and occurs in a caspase‐independent fashion. Sulfasalazine‐induced apoptosis by AIF and subsequent clearance of T‐lymphocytes might thus provide the molecular basis for the beneficial therapeutic effects of sulfasalazine in the treatment of chronic inflammatory diseases.

British Journal of Pharmacology (2002) 137, 608–620. doi:10.1038/sj.bjp.0704870
Extracellular zinc stimulates ERK‐dependent activation of p21Cip/WAF1 and inhibits proliferation of colorectal cancer cells
Authors: Park Ki‐Sook , Ahn Yongho , Kim Jin‐Ah , Yun Mi‐Sun , Seong Baik L , Choi Kang‐Yell 
Published: October 2002

Zinc is an important trace element in the body and is involved in both the proliferation and growth arrest of many kinds of cells including colorectal epithelial cells. The aim of this study was to identify the molecular mechanism of the growth regulation of colorectal cancer cells by extracellular zinc.
Zinc‐stimulated activation of the mitogen‐activated protein kinase (MAPK) cascade was measured by immunoblotting and Elk‐1 dependent trans‐reporter gene expression, and zinc‐stimulated p21Cip/WAF1 activation by immunoblotting, Northern blot analysis and immunochemistry. Cell proliferation was measured by thymidine and bromodeoxyuridine (BrdU) incorporation.
By treating colorectal cancer cells with 100 μM ZnCl2, MAPKs were activated in two different phases, the initial weak activation occurred within 5 min and this was followed by a stronger and more prolonged activation.
Zinc concomitantly activated Raf‐1‐MEK‐MAPK kinases, and induced Elk‐1 dependent trans‐reporter gene expression.
Prolonged activation of MAPKs by 100 μM of ZnCl2 resulted in the induction and nuclear localization of p21Cip/WAF1 and was related to the inhibition of both thymidine and BrdU incorporations.
These results not only suggest the presence of a mechanism for p21Cip/WAF1 dependent negative regulation of colorectal cancer cell growth by zinc but also suggest potential usage of zinc to control the growth of colorectal cancer cells.

British Journal of Pharmacology (2002) 137, 597–607. doi:10.1038/sj.bjp.0704909
Involvement of tissue kallikrein but not plasma kallikrein in the development of symptoms mediated by endogenous kinins in acute pancreatitis in rats
Authors: Griesbacher Thomas , Rainer Irmgard , Tiran Beate , Evans D Michael 
Published: October 2002

In order to investigate the mechanism of kinin release leading to vascular symptoms in acute interstitial‐oedematous pancreatitis, the novel, selective inhibitors of tissue kallikrein, (2S,2′R)‐2‐(2′‐amino‐3′‐(4′‐chlorophenyl)propanoylamino)‐N‐(3‐guanidinopropyl)‐3‐(1‐naphthyl)propanoamide (FE999024, CH‐2856), and of plasma kallikrein, (2′S,2′′R)‐4‐(2′‐(2′′(carboxymethylamino)‐3′′‐cyclohexyl‐propanoylamino)‐3′‐phenyl‐propanoylamino)piperidine‐1‐carboxamidin (FE999026, CH‐4215), were used in experimental caerulein‐induced pancreatitis in rats.
Oedema formation and plasma protein extravasation during the 2 h infusion of caerulein were inhibited in a dose‐dependent manner by i.p. pretreatment with FE999024 (7–60 μmol kg−1) while FE999026 had no effect at the same doses.
Haemoconcentration and hypovolaemia associated with the pancreatic oedema formation during pancreatitis were significantly attenuated by FE999024 at a dose of 20 μmol kg−1. The reduction in circulating plasma volume was not affected by FE999026.
Accumulation of amylase and lipase in the pancreas was dose‐dependently reduced by FE999024 while enzyme activities in the blood serum were increased by FE999024 at 60 μmol kg−1 indicating improved enzyme removal from the tissue. Enzyme activities in the tissue and in the blood remained unaffected by FE999026.
FE999024 (20 μmol kg−1) largely inhibited increased tissue kallikrein‐like activity in the pancreas during acute pancreatitis and also strongly attenuated influx of plasma kallikrein into the tissue. FE999026 (20 μmol kg−1) significantly inhibited plasma kallikrein‐like activity in the pancreas but had no effect on tissue kallikrein‐like activity.
In conclusion, vascular kinin‐mediated symptoms observed during oedematous pancreatitis in the rat are caused by the action of tissue kallikrein in the pancreas whereas an involvement of plasma kallikrein seems to be unlikely.

British Journal of Pharmacology (2002) 137, 692–700. doi:10.1038/sj.bjp.0704910
Role of the platelet‐activating factor (PAF) receptor during pulmonary infection with gram negative bacteria
Authors: Soares A C , Pinho V S , Souza D G , Shimizu T , Ishii S , Nicoli J R , Teixeira M M 
Published: October 2002

The lipid mediator PAF plays an important role in the phagocytosis of particles, including bacteria, and consequent production of pro‐inflammatory cytokines, such as TNF‐α and IL‐8.
Using a PAF receptor antagonist (UK‐74,505) and PAF receptor knock‐out mice, we have investigated the relevance of PAF for the inflammatory changes and lethality after pulmonary infection with the gram‐negative bacteria Klebsiella pneumoniae in mice.
At an inoculum of 3×106 bacteria, there was marked pulmonary (bronchoalveolar lavage and lung) neutrophilia that started early (2.5 h after infection) and peaked at 48 h. All animals were dead by day 4 of infection. The chemokine KC and the pro‐inflammatory cytokine TNF‐α increased rapidly and persisted for 48 h in the lungs.
Pretreatment with UK‐74,505 (30 mg kg−1 per day, p.o.) had no significant effects on the number of infiltrating neutrophils in BAL fluid or lung tissue, as assessed by histology and measuring myeloperoxidase, or on the concentrations of KC. In contrast, concentrations of TNF‐α and the number of bacteria inside neutrophils were significantly diminished.
In order to support a role for the PAF during K. pneumoniae infection, experiments were also carried out in PAFR‐deficient mice. In the latter animals, lethality occurred earlier than in wild‐type controls. This was associated with greater number of bacteria in lung tissue and diminished percentage of neutrophils containing bacteria in their cytoplasm.
Our results suggest that PAF, acting on its receptor, plays a protective role during infection with K. pneumoniae in mice.

British Journal of Pharmacology (2002) 137, 621–628. doi:10.1038/sj.bjp.0704918
Inotropic responses to human gene 2 (B29) relaxin in a rat model of myocardial infarction (MI): effect of pertussis toxin
Authors: Kompa Andrew R , Samuel Chrishan S , Summers Roger J 
Published: October 2002

Relaxin produces powerful inotropic and chronotropic responses in isolated atria. The effect of relaxin has been examined in a rat model of cardiac failure, induced by myocardial infarction (MI).
Maximum inotropic responses to isoprenaline (sham 5.4±0.3 mN; MI 2.6±0.3 mN; P<0.001) and relaxin (sham 5.1±0.6 mN; MI 2.8±0.5 mN; P=0.013) were reduced in left atria following MI. No change in chronotropic responsiveness was observed in right atria.
Pertussis toxin (PTX) treatment restored inotropic responses to isoprenaline (sham 5.5±1.3 mN; MI 5.8±1.0 mN; P=0.850) but not to relaxin. Instead, PTX reduced inotropic responses to relaxin in sham animals to the same level seen in the MI group (sham 3.2±1.7 mN; MI 2.8±0.6 mN; P=0.847). In right atria, PTX treatment did not affect the maximum chronotropic response to isoprenaline, but reduced responses to relaxin in both sham and MI animals.
R3 relaxin and relaxin receptor (LGR7) mRNA was present in atria and left ventricle (LV) from sham and MI animals. R3 relaxin mRNA expression was increased in atria but not LV from MI animals. LGR7 mRNA expression was reduced in atria and LV from MI animals.
PTX treatment in unoperated rats increased chronotropic responses (vehicle 184.3±5.3 beats min−1; PTX 211.3±9.5 beats min−1; P=0.029) and produced a rightward shift in the concentration‐response curve to isoprenaline in left atria. PTX reduced inotropic (vehicle 3.3±0.7 mN; PTX 0.8±0.2 mN; P=0.005) and chronotropic (vehicle 130.2±8.1 beats min−1; PTX 90.6±11.1 beats min−1; P=0.012) responses to relaxin.
In left atria, relaxin produced a small increase in cAMP compared to those produced by isoprenaline and forskolin. However, PTX treatment significantly reduced relaxin‐, isoprenaline‐ and forskolin‐stimulated cAMP accumulation.
Cardiac failure in MI animals caused a reduced inotropic response to both relaxin and (−)‐isoprenaline. In non‐MI animals, PTX treatment also reduced inotropic responses to relaxin. Differences between responses to (−)‐isoprenaline and relaxin can be explained by changes in coupling efficiency occurring at the level of adenylate cyclase.

British Journal of Pharmacology (2002) 137, 710–718. doi:10.1038/sj.bjp.0704922
Functional aspects of co‐variant surface charges in an antibody fragment
Authors: Hugo Nicolas , Lafont Virginie , Beukes Mervyn , Altschuh Danièle 
Published: October 2002

AbstractA mutational analysis of three co‐variant pairs of residues, located at the surface of a single‐chain fragment, variable (scFv), remote from the antigen‐binding site, was performed to investigate the tolerance of these positions to amino acid changes. The replacements consisted of the elimination or addition of charges, or in their replacement by a charge of opposite sign. As measured by Biacore, antigen‐binding kinetics and specificity were essentially unaffected by the mutations. The purified scFvs remained mostly 100% active for 14 h, and their sensitivity to guanidinium‐chloride denaturation was similar. These observations indicate that the mutations did not affect antigen‐binding properties and that protein folding was conserved. However, the various scFvs differed greatly in half‐life in periplasmic extracts (<4 h to >16 h at 25°C). The deleterious effect on half‐life produced by single mutations could be reversed by introducing a second mutation that restores the natural combination of amino acids in the co‐variant pair, indicating that the consequence of charge modifications at these locations depends on the sequence context. We propose that the differences in half‐life result from differences in aggregation propensities with other periplasmic proteins, related to the presence of charged patches at the surface of the scFvs. The practical implication is that changes in surface charge may drastically affect the level of active molecules in complex protein mixtures, a potentially important consideration in engineering scFvs for biotechnological or medical purposes.