bluuebunny/crossref_metadata_2025_split huggingface dataset:
A microbiological survey of communal kitchens used by undergraduate students
Authors: Sharp Kay , Walker Harriet 
Published: March 2003

AbstractThe majority of food poisoning cases occur in the domestic environment as a result of inadequate hygiene practices. The possibility of food safety errors may be increased in domestic kitchens that are shared. However, there is very little information concerning the hygiene of these kitchens. This study investigates the microbial load of key sites in six student communal kitchens. In addition, hygiene was evaluated visually and questionnaires were used to assess the hygiene practices of the kitchen users. Results show that visual hygiene assessments are not a good indicator of microbial contamination, which, in this study, reveal poor levels of hygiene. Food safety errors were commonly made by users of the kitchens and their food hygiene practices suggest limited food safety knowledge and/or an absence of feelings of responsibility for the hygiene standard of the kitchen.
A comparison and evaluation of research methods used in consumer food safety studies
Authors: Redmond Elizabeth C. , Griffith Christopher J. 
Published: March 2003

AbstractWorldwide incidence of food‐borne disease has increased in recent years and data suggest that inadequate food‐handling behaviour in the domestic environment may be an important factor. As a consequence of this, research into aspects of consumer food safety has been undertaken, especially in the UK and USA. The overall aims of conducting such research have been to investigate aspects of consumer food safety behaviour and to utilize information in the development of effective food safety education initiatives. In the past 25 years, 87 consumer food safety studies have been undertaken using different research methodologies; 75% utilized survey techniques (questionnaires and interviews), 17% were based on direct observation, and 8% utilized focus groups. The advantages and disadvantages of the different research methods used are discussed. Similarly, different forms of reliability and validity have been considered in the context of each research method used. A comparison of results from consumer food safety studies has shown that use of different research designs and approaches has resulted in differences in the findings about consumer food safety behaviour. Survey responses have provided a more optimistic portrayal of consumer food safety behaviour than data obtained from focus groups and direct observation. Although consumers have demonstrated knowledge, positive attitudes and intentions to implement safe practices, substantially larger proportions of consumers have been observed to implement frequent malpractices. This suggests that observational data provide the most reliable information denoting consumers’ actual food safety behaviour and should be used preferentially with risk‐based data for the design of communication strategies.
Brakes to organic market enlargement in Spain: consumers’ and retailers’ attitudes and willingness to pay
Authors: Sanjuán Ana I. , Sánchez Mercedes , Gil José M. , Gracia Azucena , Soler Francisco 
Published: March 2003

AbstractIn Spain, consumption of organic products has not kept pace with production. Up till now, foreign markets have been a natural destination for excess supply. However, world trade liberalization might cause important commercial problems to Spanish producers that could be partially solved by enlarging the domestic market. The goal of this paper is to assess the opportunity for such enlargement focusing on two main aspects: consumers’ and retailers’ attitudes and willingness to pay for organic products. Concerns about health, natural diets or environmental issues could stimulate consumption, while retailing dynamism and competition to gain new market segments might favour distribution. Both aspects are investigated through two surveys addressed to consumers and retailers in two Spanish towns. The results confirm that only a small proportion of consumers and distributors show attitudes that might favour demand expansion. The most sensitized segments are willing to pay more for organic products, but this premium is still very far from the prevailing gap between conventional and organic food products.
Effect of technological parameters on the characteristics of kasseri cheese made from raw or pasteurized ewes’ milk
Authors: Moatsou Golfo , Kandarakis Ioannis , Moschopoulou Ekaterini , Anifantakis Emmanouil , Alichanidis Efstathios 
Published: March 2003

Two groups of kasseri cheese (pasta filata type) were manufactured from raw or pasteurized ewes’ milk, without starter cultures. Cheeses of each group were divided into two subgroups: the first was ripened and stored at 4°C and packaged in plastic film; the second ripened and stored at 15°C and coated with paraffin wax. Milk pasteurization and technological parameters had a significant effect on the pH ( P < 0.05), while only technological parameters had an effect on the total solids content. At day 120, the range of mean cfu/g counts for the mesophilic aerobic flora was 9.5 × 107−1.4 × 108; for the thermophilic streptococci, the range was 2.6 × 107−7.6 × 107; and for the thermophilic bacilli, 9.8 × 106−1.7 × 107. Changes in the N fractions became significant after 30 days of ripening. For mature 120‐day‐old cheeses, the percentage of total N soluble at pH 4.6 was 22.7%–22.9% in raw milk cheeses and 19.0%–21.7% in pasteurized milk cheeses. The percentage of total N soluble at 12% TCA was 10.1%–12.2% in raw milk cheeses and 7.3%–11.5% in pasteurized milk cheeses; the percentages of total N soluble at 5% PTA were 3.1%–4.0% and 2.6%–3.6%, respectively. The residual αs‐casein percentages at day 120 ranged between 63% and 78% of the respective area at day 1; the residual β‐casein ranged between 67% and 75%. There were some characteristic differences in the reverse phase‐HPLC peptide profiles of the four cheeses. In general, the effect of the different ripening conditions was more pronounced in cheeses made from pasteurized milk.
Dopaminergic cell death induced by MPP+, oxidant and specific neurotoxicants shares the common molecular mechanism
Authors: . Chun Hong S , Gibson Gary E. , DeGiorgio Lorraine A. , Zhang H. , Kidd Vincent J. , Son Jin H. 
Published: March 2003

Recent etiological study in twins (Tanneret al. 1999) strongly suggests that environmental factors play an important role in typical, non‐familial Parkinson's disease (PD), beginning after age 50. Epidemiological risk factor analyses of typical PD cases have identified several neurotoxicants, including MPP+(the active metabolite of MPTP), paraquat, dieldrin, manganese and salsolinol. Here, we tested the hypothesis that these neurotoxic agents might induce cell death in our nigral dopaminergic cell line, SN4741 (Sonet al. 1999) through a common molecular mechanism. Our initial experiments revealed that treatment with both MPP+and the other PD‐related neurotoxicants induced apoptotic cell death in SN4741 cells, following initial increases of H2O2‐related ROS activity and subsequent activation of JNK1/2 MAP kinases. Moreover, we have demonstrated that during dopaminergic cell death cascades, MPP+, the neurotoxicants and an oxidant, H2O2equally induce the ROS‐dependent events. Remarkably, the oxidant treatment alone induced similar sequential molecular events: ROS increase, activation of JNK MAP kinases, activation of the PITSLRE kinase, p110, by both Caspase‐1 and Caspase‐3‐like activities and apoptotic cell death. Pharmacological intervention using the combination of the antioxidant Trolox and a pan‐caspase inhibitor Boc‐(Asp)‐fmk (BAF) exerted significant neuroprotection against ROS‐induced dopaminergic cell death. Finally, the high throughput cDNA microarray screening using the current model identified downstream response genes, such as heme oxygenase‐1, a constituent of Lewy bodies, that can be the useful biomarkers to monitor the pathological conditions of dopaminergic neurons under neurotoxic insult.
Inhibition of tumour necrosis factor‐α (TNFα)‐induced NF‐κB p52 converts the metabolic effects of microglial‐derived TNFα on mouse cerebellar neurones to neurotoxicity
Authors: Nicholas Richard St J. , Compston Alastair , Brown David R. 
Published: March 2003

Activated microglia are implicated in the injury of neurones and macroglia bothin vitroandin vivo.Here, we demonstrate that media conditioned by interferon‐γ treated microglia initially impair the metabolism of mouse cerebellar neurones grown in serum‐free conditions without inducing cell death. Metabolic effects include inhibition of the ability of mitochondria to reduce 3‐[4,5‐dimethylthiazol‐2‐yl]‐2,5‐diphenyltetrazolium bromide (MTT) and cytochrome oxidase activity. These effects are blocked by antibodies to tumour necrosis factor‐α (TNFα), a cytokine produced by microglial activation, and they are not reproduced by media conditioned by resting microglia. The metabolic effects are evident for up to 24 hin vitro. More prolonged exposure, up to 48 h, results in TNFα dependent neuronal death as previously observed. Between 2 and 48 h TNFα present in media conditioned by interferon‐γ treated but not resting microglia is associated with nuclear factor kappa B (NF‐κB) consensus sequence binding in paired mouse cerebellar neuronal cultures without affecting activation of the signal transducer and activator of transcription (STAT) transcription factor. Neuronal death can be accelerated by peptide blockade of the nuclear transport of NF‐κB p52 subunit during exposure of cerebellar neurones to medium from interferon‐γ treated microglia. This toxicity is blocked by anti‐TNFα antibody. Soluble factors released by activated microglia therefore contribute to neuronal dysfunction that is initially reversible but may culminate in neurotoxicity. Characterizing and manipulating these eventsin vivotheoretically provides an opportunity for neuroprotection in selected diseases affecting the central nervous system.
Plasmalogen deficiency in early Alzheimer's disease subjects and in animal models: molecular characterization using electrospray ionization mass spectrometry
Authors: Han Xianlin , Holtzman David M. , McKeel Daniel W. 
Published: March 2003

To explore the hypothesis that alterations in ethanolamine plasmalogen may be directly related to the severity of dementia in Alzheimer's disease (AD), we performed a systematic examination of plasmalogen content in cellular membranes of gray and white matter from different regions of human subjects with a spectrum of AD clinical dementia ratings (CDR) using electrospray ionization mass spectrometry (ESI/MS). The results demonstrate: (1) a dramatic decrease in plasmalogen content (up to 40 mol% of total plasmalogen) in white matter at a very early stage of AD (i.e. CDR 0.5); (2) a correlation of the deficiency in gray matter plasmalogen content with the AD CDR (i.e. ∼10 mol% of deficiency at CDR 0.5 (very mild dementia) to ∼30 mol% of deficiency at CDR 3 (severe dementia); (3) an absence of alterations of plasmalogen content and molecular species in cerebellar gray matter at any CDR despite dramatic alterations of plasmalogen content in cerebellar white matter. Alterations of ethanolamine plasmalogen content in two mouse models of AD, APPV717F and APPsw, were also examined by ESI/MS. A plasmalogen deficiency was present (up to 10 mol% of total plasmalogen at the age of 18 months) in cerebral cortices, but was absent in cerebella from both animal models. These results suggest plasmalogen deficiency may play an important role in the AD pathogenesis, particularly in the white matter, and suggest that altered plasmalogen content may contribute to neurodegeneration, synapse loss and synaptic dysfunction in AD.
Enhanced inducible mGlu1α receptor expression in Chinese hamster ovary cells
Authors: Nash Mark S. , Selkirk Julie V. , Gaymer Caroline E. , Challiss R. A. John , Nahorski Stefan R. 
Published: March 2003

Inducible expression of the group‐I metabotropic glutamate receptor (mGlu1α) in Chinese hamster ovary cells allows for the study of receptor density dependent effects. However, expression levels attainable with this system are lower than those reported for various brain regions and achieved by conventional (constitutive) transfection. Thus, direct comparison of mGlu1α receptor‐mediated responses in this inducible expression system with those for receptors expressed heterologously or in vivo is compounded. We show here that inducible expression can be selectively augmented by butyrate pretreatment to levels approaching those reported for cerebral tissue. Enhanced mGlu1α receptor protein levels, agonist‐induced inositol phosphate accumulation, as well as single‐cell inositol 1,4,5‐trisphosphate production and intracellular Ca2+ mobilization occurred following co‐induction with butyrate. In contrast, endogenous purinoceptor function was unaffected. Importantly, the ability to titrate receptor expression by varying isopropyl β‐thiogalactoside concentration was retained. Sodium butyrate thus offers a simple and convenient method to enhance inducible gene expression to levels found in vivo.
Lithium inhibits caspase 3 activation and dephosphorylation of PKB and GSK3 induced by K+deprivation in cerebellar granule cells
Authors: Mora Alfonso , Sabio Guadalupe , González‐Polo Rosa A. , Cuenda Ana , Alessi Dario R. , Alonso Juan C. , Fuentes José M. , Soler Germán , Centeno Francisco 
Published: March 2003

Lithium protects cerebellar granule cells from apoptosis induced by low potassium, and also from other apoptotic stimuli. However, the precise mechanism by which this occurs is not understood. When cerebellar granule cells were switched to low potassium medium, the activation of caspase 3 was detected within 6 h, suggesting a role of caspase 3 in mediating apoptosis under conditions of low potassium. In the same conditions, lithium (5 mm) inhibited the activation of caspase 3 induced by low potassium. As lithium did not inhibit caspase 3 activityin vitro, these results suggest that this ion inhibits an upstream component that is required for caspase 3 activation. Lithium is known to inhibit a kinase termed glycogen sythase kinase 3 (GSK3), which is implicated in the survival pathway of phosphatidylinositol 3‐kinase/protein kinase B (PI3K/PKB). Here we demonstrate that low potassium in the absence of lithium induces the dephosphorylation, and therefore the activation, of GSK3. However, when lithium was present, GSK3 remained phosphorylated at the same level as observed under conditions of high potassium. Low potassium induced the dephosphorylation and inactivation of PKB, whereas when lithium was present PKB was not dephosphorylated. Our results allow us to propose a new hypothesis about the action mechanism of lithium, this ion could inhibit a serine‐threonine phosphatase induced by potassium deprivation.
Calcium and pituitary adenylate cyclase‐activating polypeptide induced expression of circadian clock gene mPer1 in the mouse cerebellar granule cell culture
Authors: Akiyama Masashi , Minami Youichi , Nakajima Tatsuki , Moriya Takahiro , Shibata Shigenobu 
Published: March 2003

Mammalian circadian clock genes Per1 and Per2 are rhythmically expressed not only in the suprachiasmatic nucleus where the mammalian circadian clock exists, but also in other brain regions and peripheral tissues. The induced circadian oscillation of Per genes after treatment with high concentrations of serum or various drugs in cultured cells suggests the ubiquitous existence of the oscillatory mechanism. These treatments also result in a rapid surge of expression of Per1. It has been shown that multiple signaling pathways are involved in Per1 gene induction in culture cells. We used a dispersed primary cell culture made up of mouse cerebellar granule cells to examine the stimuli inducing the mPer genes and their signaling pathways in neuronal tissues expressing mPer genes. We demonstrated that mPer1, but not mPer2, mRNA expression was dependent on the depolarization state controlled by extracellular KCl concentration in the granule cell culture. Nifedipine treatment reduced mPer1 induction, suggesting that mPer1 mRNA expression depends on intracellular calcium concentration regulated through a voltage‐dependent Ca2+ channel. Transient mPer1 mRNA induction was observed after elevating KCl concentration in the medium from 5 mm to 25 mm. This increased expression was suppressed by a calmodulin antagonist, or CaMKII/IV inhibitor, but not by MEK inhibitors. Addition of pituitary adenylate cyclase‐activating polypeptide‐38 to the medium also induced transient Per1 gene expression. This induction was mimicked by dibutyryl‐cAMP and suppressed by a protein kinase A (PKA) inhibitor, but not by MEK inhibitors. These results suggest that Ca2+/calmodulin‐dependent protein kinase II/IV‐ and PKA‐dependent pathways are involved in high‐KCl and PACAP‐induced mPer1 induction, respectively, and neural tissues use multiple signaling pathways for mPer1 induction similar to culture cells.
Aberrant metal binding by prion protein in human prion disease
Authors: Wong Boon‐Seng , Chen Shu G. , Colucci Monica , Xie Zhiliang , Pan Tao , Liu Tong , Li Ruliang , Gambetti Pierluigi , Sy Man‐Sun , Brown David R. 
Published: March 2003

Human prion diseases are characterized by the conversion of the normal prion protein (PrPC) into a pathogenic isomer (PrPSc). Distinct PrPSc conformers are associated with different subtypes of prion diseases. PrPC binds copper and has antioxidation activity. Changes in metal‐ion occupancy can lead to significant decline of the antioxidation activity and changes in conformation of the protein. We studied the trace element status of brains from patients with sporadic Creutzfeldt–Jakob disease (sCJD). We found a decrease of up to 50% of copper and an increase in manganese of approximately 10‐fold in the brain tissues from sCJD subjects. We have also studied the metal occupancy of PrP in sCJD patients. We observed striking elevation of manganese and, to a lesser extent, of zinc accompanied by significant reduction of copper bound to purified PrP in all sCJD variants, determined by the PrP genotype and PrPSc type, combined. Both zinc and manganese were undetectable in PrPC preparations from controls. Copper and manganese changes were pronounced in sCJD subjects homozygous for methionine at codon 129 and carrying PrPSc type‐1. Anti‐oxidation activity of purified PrP was dramatically reduced by up to 85% in the sCJD variants, and correlated with increased in oxidative stress markers in sCJD brains. These results suggest that altered metal‐ion occupancy of PrP plays a pivotal role in the pathogenesis of prion diseases. Since the metal changes differed in each sCJD variants, they may contribute to the diversity of PrPSc and disease phenotype in sCJD. Finally, this study also presented two potential approaches in the diagnosis of CJD; the significant increase in brain manganese makes it potentially detectable by MRI, and the binding of manganese by PrP in sCJD might represent a novel diagnostic marker.
Adenosine in the central nervous system: release mechanisms and extracellular concentrations
Authors: Latini Serena , Pedata Felicita 
Published: March 2003

Adenosine has several functions within the CNS that involve an inhibitory tone of neurotransmission and neuroprotective actions in pathological conditions. The understanding of adenosine production and release in the brain is therefore of fundamental importance and has been extensively studied. Conflicting results are often obtained regarding the cellular source of adenosine, the stimulus that induces release and the mechanism for release, in relation to different experimental approaches used to study adenosine production and release. A neuronal origin of adenosine has been demonstrated through electrophysiological approaches showing that neurones can release significant quantities of adenosine, sufficient to activate adenosine receptors and to modulate synaptic functions. Specific actions of adenosine are mediated by different receptor subtypes (A1, A2A, A2B and A3), which are activated by various ranges of adenosine concentrations. Another important issue is the measurement of adenosine concentrations in the extracellular fluid under different conditions in order to know the degree of receptor stimulation and understand adenosine central actions. For this purpose, several experimental approaches have been used both in vivo and in vitro, which provide an estimation of basal adenosine levels in the range of 50–200 nm. The purpose of this review is to describe pathways of adenosine production and metabolism, and to summarize characteristics of adenosine release in the brain in response to different stimuli. Finally, studies performed to evaluate adenosine concentrations under physiological and hypoxic/ischemic conditions will be described to evaluate the degree of adenosine receptor activation.
Cytosolic O‐glycosylation is abundant in nerve terminals
Authors: Cole Robert N. , Hart Gerald W. 
Published: March 2003

Phosphorylation plays a key role in regulating growth cone migration and protein trafficking in nerve terminals. Here we show that nerve terminal proteins contain another abundant post‐translational modification: β‐N‐acetylglucosamine linked to hydroxyls of serines or threonines (O‐GlcNAc1). O‐GlcNAc modifications are essential for embryogenesis and mounting evidence suggests that O‐GlcNAc is a regulatory modification that affects many phosphorylated proteins. We show that the activity and expression of O‐GlcNAc transferase (OGT) and N‐acetyl‐β‐d‐glucosaminidase (O‐GlcNAcase), the two enzymes regulating O‐GlcNAc modifications, are present in nerve terminal structures (synaptosomes) and are particularily abundant in the cytosol of synaptosomes. Numerous synaptosome proteins are highly modified with O‐GlcNAc. Although most of these proteins are present in low abundance, we identified by proteomic analysis three neuron‐specific O‐GlcNAc modified proteins: collapsin response mediator protein‐2 (CRMP‐2), ubiquitin carboxyl hydrolase‐L1 (UCH‐L1) and β‐synuclein. CRMP‐2, which is involved in growth cone collapse, is a major O‐GlcNAc modified protein in synaptosomes. All three proteins are implicated in regulatory cascades that mediate intracellular signaling or neurodegenerative diseases. We propose that O‐GlcNAc modifications in the nerve terminal help regulate the functions of these and other synaptosome proteins, and that O‐GlcNAc may play a role in neurodegenerative disease.