bluuebunny/crossref_metadata_2025_split huggingface dataset:
Reproducibility of sphero‐cylindrical prescriptions*
Authors: MacKenzie Graeme E. 
Published: March 2008

AbstractPurpose:  To investigate the reproducibility of the sphero‐cylindrical prescriptions provided by 40 optometrists.Methods:  Forty registered optometrists were randomly selected from the cities of Oxford and Westminster in the UK to perform a sphero‐cylindrical refraction on an asymptomatic 29‐year‐old male subject. The 95% limits of reproducibility for each component of refraction were assessed and are presented together with scatterplots, distribution ellipsoids and polar profiles of dioptric power.Results:  The mean stigmatic (spherical equivalent) refraction for the right eye was −0.83 D (S.D. = 0.28 D) with 95% limits of agreement −1.38 and −0.28 D. The 95% reproducibility limits for stigmatic data [] was 0.78 D. The average inter‐ocular difference in the stigmatic components of refraction was −0.044 D (S.D. = 0.20 D) but estimates ranged from −0.50 to +0.50 D. Mean ortho‐ and oblique antistigmatic refractions were −0.23 D (S.D. = 0.084 D) and −0.14 D (S.D. = 0.086 D) respectively.Conclusions:  The findings of this paper suggest that refractions performed by multiple optometrists on a single eye will differ in their stigmatic component by over 0.78 D on average not more than once in 20 refractions. The reproducibility of refractions reported here, approximately twice as variable as those reported under repeatability conditions, has profound implications for the analysis of refractive data collected by multiple optometrists over the course of replication, longitudinal and epidemiological studies.
Strain Differences in Alcohol‐Induced Neurochemical Plasticity: A Role for Accumbens Glutamate in Alcohol Intake
Authors: Kapasova Zuzana , Szumlinski Karen K. 
Published: March 2008

Background: Repeated alcohol administration alters nucleus accumbens (NAC) basal glutamate content and sensitizes the capacity of alcohol to increase NAC extracellular glutamate levels. However, the relevance of alcohol‐induced changes in NAC glutamate for alcohol drinking behavior is under‐investigated.Methods: To examine the relationship between genetic variance in alcohol consumption and alcohol‐induced neuroadaptations within the NAC, in vivo microdialysis was conducted in the alcohol‐preferring C57BL/6J (B6) and alcohol‐avoiding DBA2/J (D2) mouse strains on injections 1 and 8 of repeated alcohol treatment (8 × 2 g/kg, IP). To confirm an active role for NAC glutamate in regulating alcohol drinking behavior, the glutamate reuptake inhibitordl‐threo‐β‐benzyloxyaspartic acid (TBOA) (300 μM) and the Group 2 metabotropic glutamate autoreceptor agonist (2R,4R)‐4‐aminopyrrolidine‐2,4‐dicarboxylate (APDC) (50 μM) were infused into the NAC of B6 and D2 mice prior to alcohol consumption in a 4 bottle‐choice test.Results: While strain differences were not apparent for NAC basal levels of dopamine, serotonin or γ‐amino butyric acid (GABA), repeated alcohol treatment elevated NAC basal glutamate content only in B6 mice. Strain differences in both the acute and the sensitized neurochemical responses to 2 g/kg alcohol were observed for all neurotransmitters examined. While the alcohol‐induced rise in NAC dopamine and glutamate levels sensitized in B6 mice, a sensitization was not observed in D2 animals. Moreover, B6 mice exhibited a sensitized serotonin and GABA response to alcohol followed repeated treatment, whereas neither tolerance nor sensitization was observed in D2 animals. An intra‐NAC APDC infusion reduced alcohol intake in both B6 and D2 mice by approximately 50%. In contrast, TBOA infusion elevated alcohol intake selectively in B6 mice.Conclusions: These data indicate an active role for NAC glutamate in regulating alcohol consumption in mice and support the hypothesis that predisposition to high alcohol intake involves genetic factors that facilitate alcohol‐induced adaptations in glutamate release within the NAC.
Patterns of Alcohol Consumption and Alcohol‐Impaired Driving in the United States
Authors: Flowers Nicole T. , Naimi Timothy S. , Brewer Robert D. , Elder Randy W. , Shults Ruth A. , Jiles Ruth 
Published: March 2008

Background: Alcohol‐related motor vehicle crashes kill approximately 17,000 Americans annually and were associated with more than $51 billion in total costs in 2000. Relatively little is known about the drinking patterns of alcohol‐impaired (AI) drivers in the United States.Methods: 2006 Behavioral Risk Factor Surveillance System (BRFSS) was analyzed for alcohol consumption and self‐reported AI driving among U.S. adults aged ≥18 years for all states. Alcohol consumption was divided into 4 categories: binge/heavy, binge/nonheavy, nonbinge/heavy, and nonbinge/nonheavy. Binge drinking was defined as ≥5 drinks for men or ≥4 drinks for women on one or more occasions in the past month, and heavy drinking was defined as average daily consumption of >2 drinks/day (men) or >1 drink/day (women). The prevalence of AI driving was examined by drinking pattern and by demographic characteristics. Logistic regression analysis was used to assess the association between drinking patterns and AI driving.Results: Five percent of drinkers were engaged in AI driving during the past 30 days. Overall, 84% of AI drivers were binge drinkers and 88% of AI driving episodes involved binge drinkers. By drinking category, binge/nonheavy drinkers accounted for the largest percentage of AI drivers (49.4%), while binge/heavy drinkers accounted for the most episodes of AI driving (51.3%). The adjusted odds of AI driving were 20.1 (95% CI: 16.7, 24.3) for binge/heavy, 8.2 (6.9, 9.7) for binge/nonheavy, and 3.9 (2.4, 6.3) for nonbinge/heavy drinkers, respectively.Conclusions: There is a strong association between binge drinking and AI driving. Most AI drivers and almost half of all AI driving episodes involve persons who are not heavy drinkers (based on average daily consumption). Implementing effective interventions to prevent binge drinking could substantially reduce AI driving.
Adipose Differentiation‐Related Protein Is a Reliable Lipid Droplet Marker in Alcoholic Fatty Liver of Rats
Authors: Mak Ki M. , Ren Chaoling , Ponomarenko Anatoly , Cao Qi , Lieber Charles S. 
Published: March 2008

Background:  Adipose differentiation‐related protein (ADRP) is a lipid droplet‐associated protein that coats cytoplasmic lipid droplets. The present study evaluated whether alcohol feeding enhances ADRP expression and whether ADRP is a lipid droplet marker in alcoholic fatty liver of rats. Because medium‐chain triglycerides (MCT) reduce alcoholic hepatosteatosis, their effects on ADRP were also evaluated.Methods:  Fatty liver was induced in rats by the consumption of the Lieber‐DeCarli alcohol liquid diet with or without replacement of long‐chain triglycerides (LCT) by MCT (32% of calories). Immunohistochemical staining for ADRP was performed in formalin‐fixed, paraffin‐embedded liver sections. ADRP immunostaining was quantified by image analysis. Triacylglycerol was measured chemically. ADRP mRNA and protein were analyzed by real‐time polymerase chain reaction and western blot, respectively. Double staining technique was performed to distinguish ADRP from glycogen in hepatocytes.Results:  Alcohol feeding for 21 days increased ADRP staining in the centrilobular and mid zonal regions of the liver lobules coincident with fat deposition in the liver. Replacing LCT in the alcohol diet with MCT diminished ADRP immunostaining in parallel with reduced steatosis. MCT also attenuated the up‐regulation of ADRP mRNA and protein after alcohol. In steatotic hepatocytes ADRP selectively stained the surface of macrovesicular and microvesicular lipid droplets. ADRP immunostaining quantitatively correlated with hepatic triacylglycerol levels, validating ADRP as a reliable lipid droplet marker. Compared with hematoxylin and eosin stains, ADRP was more sensitive in detecting microvesicular lipid droplets. ADRP immunostaining also distinguished lipid droplets from glycogen, as demonstrated by double staining for ADRP and glycogen.Conclusions:  Alcohol induction of fatty liver enhances ADRP expression and MCT oppose the alcohol effects. ADRP is a reliable and sensitive marker for lipid droplets in alcoholic fatty liver. ADRP immunostaining permits quantification of fatty change in hepatocytes and can be used as an ancillary technique in assessing the efficacy of diets or drugs against hepatosteatosis.
Ethanol Selectively Attenuates NMDAR‐Mediated Synaptic Transmission in the Prefrontal Cortex
Authors: Weitlauf Carl , Woodward John J. 
Published: March 2008

Background:  Brain imaging studies have revealed abnormal function in the prefrontal cortex (PFC) of alcoholics that may contribute to the impulsive behavior and lack of control over drinking that characterizes this disorder. Understanding how ethanol affects the physiology of PFC neurons may help explain this loss of control and lead to better treatments for alcohol addiction. In a previous study from this laboratory, we showed that ethanol inhibits complex patterns of persistent activity (known as “up‐states”) in medial PFC (mPFC) neurons in a reversible and concentration‐dependent manner.Methods:  In the current study, whole‐cell patch clamp recordings were used to directly examine the effects of ethanol on the glutamatergic and GABAergic components that underlie persistent activity.Results:  In deep‐layer mPFC pyramidal neurons, ethanol reversibly attenuated electrically evoked N‐methyl‐d‐aspartate‐type glutamate receptor (NMDAR)‐mediated EPSCs. Significant inhibition was observed at concentrations as low as 22 mM, equivalent to a blood ethanol concentration (0.1%) typically associated with legal limits for intoxication. In contrast to NMDA responses, neither evoked nor spontaneous EPSCs mediated by α‐amino‐3‐hydroxy‐5‐methylisoxazole‐4‐propionic acid‐type glutamate receptor were affected by ethanol at concentrations as high as 88 mM, a concentration that can be fatal to non‐tolerant individuals. At similar concentrations, ethanol also had little effect on spontaneous or evoked IPSCs mediated by a‐type γ‐aminobutyric acid receptor. Finally, mPFC neurons showed little evidence of GABAR‐mediated tonic current and this was unaffected by ethanol.Conclusions:  Together, these results suggest that NMDAR‐mediated processes in the mPFC may be particularly susceptible to disruption following the acute ingestion of ethanol.
Na,K‐ATPase Expression Is Increased in the Lungs of Alcohol‐Fed Rats
Authors: Otis Jeffrey S. , Mitchell Patrick O. , Kershaw Corey D. , Joshi Pratibha C. , Guidot David M. 
Published: March 2008

Background:  Alcohol abuse independently increases the risk of developing the acute respiratory distress syndrome (ARDS), a disease characterized by diffuse alveolar epithelial damage, lung edema, and consequent severe hypoxemia. Chronic alcohol abuse increases alveolar epithelial permeability both in vitro and in vivo, in part due to altered tight junction formation. However, both alcohol‐fed animals and otherwise healthy alcoholic humans do not have pulmonary edema at baseline, even though their lungs are highly susceptible to acute edematous injury in response to inflammatory stresses. This suggests that active fluid transport by the alveolar epithelium is preserved or even augmented in the alcoholic lung. Chronic alcohol ingestion increases expression of apical sodium channels in the alveolar epithelium; however, its effects on the Na,K‐ATPase complex that drives sodium and fluid transport out of the alveolar space have not been examined.Methods:  Age‐ and gender‐matched Sprague–Dawley rats were fed the Lieber–DeCarli liquid diet containing either alcohol or an isocaloric substitution (control diet) for 6 weeks. Gene and protein expression of lung Na,K‐ATPase α1, α2, and β1 subunits were quantified via real‐time PCR and immunobiological analyses, respectively. Alcohol‐induced, Na,K‐ATPase‐dependent epithelial barrier dysfunction was determined by calculating lung tissue wet:dry ratios following an ex vivo buffer‐perfused challenge for 2 hours in the presence of ouabain (10−4 M), a Na,K‐ATPase inhibitor.Results:  Chronic alcohol ingestion significantly increased gene and protein expression of each Na,K‐ATPase subunit in rat lungs. Immunohistochemical analyses of the alcoholic lung also revealed that protein expression of the Na,K‐ATPase α1 subunit was increased throughout the alveolar epithelium. Additionally, lungs isolated from alcohol‐fed rats developed more edema than comparably treated lungs from control‐fed rats, as reflected by increased lung tissue wet:dry ratios.Conclusions:  These findings indicate that chronic alcohol ingestion, which is known to increase alveolar epithelial paracellular permeability, actually increases the expression of Na,K‐ATPase in the lung as a compensatory mechanism. This provides a potential explanation as to why the otherwise healthy alcoholic does not have evidence of pulmonary edema at baseline.
Infection with an insect virus affects olfactory behaviour and interactions with host plant and natural enemies in an aphid
Authors: Ban Liping , Ahmed Elham , Ninkovic Velemir , Delp Gabriele , Glinwood Robert 
Published: March 2008

AbstractAphid ecology and population dynamics are affected by a series of factors including behavioural responses to ecologically relevant chemical cues, capacity for population growth, and interactions with host plants and natural enemies. Using the aphid Rhopalosiphum padi (L.) (Homoptera: Aphididae), we showed that these factors were affected by infection with Rhopalosiphum padi virus (RhPV). Uninfected aphids were attracted to odour of uninfected aphids on the host plant, an aggregation mechanism. However, infected aphids were not attracted, and neither infected nor uninfected aphids were attracted to infected aphids on the plant. Infected aphids did not respond to methyl salicylate, a cue denoting host suitability. Infected aphids were more behaviourally sensitive to aphid alarm pheromone, and left the host plant more readily in response to it. RhPV reduced the lifespan and population growth rate of the aphid. The predacious ladybird, Coccinella septempunctata (L.) (Coleoptera: Coccinellidae), consumed more infected aphids than uninfected aphids in a 24‐h period, and the aphid parasitoid Aphidius ervi Haliday (Hymenoptera: Aphidiidae) attacked more infected than uninfected aphids. However, the proportion of mummies formed was lower with infected aphids. The results represent further evidence that associated organisms can affect the behaviour and ecology of their aphid hosts.
Association between alcohol consumption and dental health
Authors: Jansson Leif 
Published: March 2008

AbstractObjectives: To study the association of alcohol consumption with dental health in a sample from the County of Stockholm.Material and Methods: In a longitudinal investigation, 513 individuals were examined in 1970 and 1990. Clinical and radiographic examinations were performed as well as an interview including questions on alcohol consumption. The clinical investigation consisted of the registration of the number of remaining teeth, dental restorations, caries and periodontal conditions. The marginal bone level and longitudinal bone loss were determined by assessments on the proximal surfaces of all measurable teeth on the radiographs. Stepwise multiple regression analyses were adopted to calculate the partial correlations between alcohol consumption and the investigated odontological variables.Results: The group of subjects with the highest alcohol consumption (>5 cl pure alcohol per day) had more tooth surfaces with caries, more calculus and more teeth with apical lesions compared with those who reported an alcohol consumption 5 cl of pure alcohol per day. Alcohol consumption was not associated with periodontal disease.Conclusion: The observations do not support any association between alcohol consumption and periodontal disease. However, individuals with high alcohol consumption had significantly more teeth with decayed surfaces and apical lesions indicating that lifestyle‐related factors may influence dental health.
Staphylococcal enterotoxin B enhances a flare‐up reaction of murine contact hypersensitivity through up‐regulation of interferon‐γ
Authors: Miyata Akiko , Natsuaki Masaru , Yamanishi Kiyofumi 
Published: March 2008

AbstractBackground:  We often see aggravation of eczematous skin lesions associated with bacterial infection, but the mechanism of this phenomenon is unclear. Staphylococcus aureus is known to colonize on the eczematous lesion and produce some exotoxins, which act as bacterial superantigens.Objectives:  To investigate the potential role of superantigens in chronic dermatitis, we investigated the effect of staphylococcal enterotoxin B (SEB) on the skin reaction, the proliferative response and the cytokine production of local lymph node cells in the mouse model of contact hypersensitivity reaction.Methods:  Sensitized BALB/c mice were repeatedly challenged with dinitrofluorobenzene (DNFB), and intravenously injected with SEB and dinitrobenzne sulfonic acid sodium salt (DNBS). The ear swelling response was measured after DNBS injection. Cervical lymph node cells of those mice were cultured with DNBS in vitro. Their proliferative responses and the production of cytokines were assessed.Results:  SEB markedly enhanced the flare‐up reaction of ear swelling induced by DNBS, the proliferative response of lymph node cells and the production of IFN‐γ. In contrast, the production of IL‐5 was decreased.Conclusions:  The present study may provide some clues for elucidating the mechanism involved in the exacerbation of dermatitis associated with staphylococcal infection.
Magnetic resonance imaging findings in Hunter syndrome
Authors: Finn Chelsea T , Vedolin Leonardo , Schwartz Ida V , Giugliani Roberto , Haws Charlotte A , Prescot Andrew P , Renshaw Perry F 
Published: March 2008

AbstractHunter syndrome is a rare genetic lysosomal storage disease that is caused by a deficiency, or absence, of iduronate‐2‐sulphatase, an enzyme needed to break down specific glycosaminoglycans (GAGs). As a result, GAGs build up in various tissues throughout the body leading to adverse neurological and non‐neurological effects. This literature review focuses on the neurological findings. Although few magnetic resonance imaging studies have been conducted, those done have shown that patients with Hunter syndrome generally exhibit brain atrophy, enlarged periventricular spaces and ventriculomegaly. Similar findings have been reported in other mucopolysaccharide disorders. Enzyme replacement therapy is a novel treatment which has had success in treating peripheral disease in mice and humans.Conclusion: Future studies should focus on how structural and chemical signatures in the brain of Hunter patients are altered before and after enzyme replacement therapy, and how those alterations correlate with clinical outcome.
Metachromatic leukodystrophy: genetics, pathogenesis and therapeutic options
Authors: Gieselmann Volkmar 
Published: March 2008

AbstractMetachromatic leukodystrophy is a lysosomal storage disease caused by the deficiency of arylsulphatase A (ASA). This leads to storage of the membrane lipid sulphatide, which is abundant in myelin. A pathological hallmark of the disease is demyelination, causing various and ultimately lethal neurological symptoms. Today more than 110 mutations in the ASA gene have been identified, of which only three are frequent. Patients homozygous for alleles, which do not allow for the synthesis of functional ASA always suffer from the severe form of the disease, whereas alleles allowing the expression of residual enzyme activity are associated with the later onset juvenile or adult forms of metachromatic leukodystrophy. In addition, there are other as yet unknown genetic or epigenetic factors modifying the phenotype substantially. ASA‐deficient mice have been generated as a model of metachromatic leukodystrophy. These mice store sulphatide and show progressive neurological symptoms, but do not demyelinate. This animal model was recently improved using a transgenic approach, which generated mice in which sulphatide synthesis in myelin‐producing cells is enhanced. This new animal model reflects the pathological characteristics of the human disease. ASA‐deficient mice have been used in various therapeutic trials involving enzyme replacement, haematopoietic stem‐cell‐based gene therapy and direct injections of ASA‐expressing viral vectors into the brain. These animal studies have paved the way for future clinical studies of enzyme replacement and gene therapy.Conclusion: For many years this devastating disorder was considered untreatable and the outlook for patients was poor. Within a comparatively short period of time since the ASA gene was cloned in 1989, genetic and biochemical studies and data generated from newly developed animal models have led to the first clinical trials. It is hoped that these developments will prove beneficial for patients.
Enzyme replacement therapy with idursulfase in patients with mucopolysaccharidosis type II
Authors: Wraith J Edmond 
Published: March 2008

AbstractMucopolysaccharidosis type II (MPS II; Hunter syndrome) is a rare X‐linked recessive disease caused by deficiency of the lysosomal enzyme iduronate‐2‐sulphatase. This leads to the progressive accumulation of glycosaminoglycans in tissues throughout the body. As a result, patients may suffer from severe airway obstruction, skeletal deformities, cardiomyopathy and, in severely affected patients, there may be progressive neurological decline. Despite the early onset of signs and symptoms, diagnosis is often delayed. Until recently, treatment for MPS II has been largely palliative; however, enzyme replacement therapy with recombinant iduronate‐2‐sulphatase, which is produced in a human cell line and targets the underlying cause of the disease, has now been approved.Conclusion: This short review provides an overview of the natural history of MPS II and current experience of enzyme replacement therapy with idursulfase.
Pilot study to assess the validity of the single assessment process as a screening tool for dental treatment needs in older people
Authors: Heyes Gill , Robinson Peter G. 
Published: March 2008

Objective:  To assess the feasibility of using a questionnaire‐based needs assessment tool (D‐E‐N‐T‐A‐L) to screen for dental treatment need as part of the single assessment process (SAP) for older people in Sheffield.Materials and methods:  Test validation study comparing questionnaire‐assessed and normative need in two consecutive samples of older adults: 48 living at home in the transition phase of older age and 29 frail older adults living in care homes. Each answered the six D‐E‐N‐T‐A‐L questions as part of SAP and a dental examination was carried out within 2 weeks in participants’ homes. Question‐defined need was then compared to the normative need.Results:  Questionnaire‐defined and normative need were high in both the transitional group (83% and 90% respectively) and the frail group (83% and 62%). These high levels of need meant that the sensitivity and positive predictive values of D‐E‐N‐T‐A‐L were high, but the specificity and negative predictive values were low.Conclusion:  The high levels of need in these patient groups suggests that preliminary questionnaire‐based screening is an unnecessary step. A clinical examination of all older people undergoing SAP may be necessary. Further research may be warranted on the use of questionnaires to assess dental treatment needs among people with different attendance patterns.