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Y Andersson

Publications and source records attributed to Y Andersson.

At least 37 records · Page 2Linked to original sources
PubMed2000

A summary of reported foodborne disease incidents in Sweden, 1992 to 1997.

Reports of foodborne disease incidents in Sweden from 1992 to 1997 are summarized. The results are based on reports from the municipal environmental and public health authorities to the National Food Administration and from medical authorities to the Swedish Institute for Infectious Diseases Control. A total of 555 incidents, of which 84% were outbreaks, were reported, involving 11,076 ill people. In 66% of the incidents, no disease agent was determined. Bacterial agents were implicated in 25% and viruses in 8% of the incidents. Calicivirus was the most reported agent both in terms of incidents and cases. Mixed dishes was the food category most often implicated in outbreaks, and smorgasbord and casserole or stews were the subcategories that caused the most cases. The place of consumption was unknown in 8% of the incidents. In about 60% of the incidents, the implicated food was consumed in commercial food establishments; in approximately 20% of incidents, it was consumed at home. The average annual incidence of reported foodborne disease in Sweden was estimated to be 21 cases per 100,000. The average annual incidence of reported foodborne salmonellosis and campylobacteriosis was estimated to be 2.0 and 0.6 cases per 100,000, respectively. The awareness and motivation to report foodborne diseases need to be improved, but additional sources of information are needed to counteract some of the limitations of reporting discussed in this work.

Caliciviridae↗
PubMed1999

The risk of Guillain-Barré syndrome following infection with Campylobacter jejuni.

To estimate the incidence of Guillain-Barré syndrome (GBS) following Campylobacter jejuni infection (CI) we studied three populations where outbreaks of CI had occurred involving an estimated 8000 cases. No case of GBS was detected in the 6 months following the outbreaks in the local populations. The point estimate for the risk of GBS following CI estimated in this study was 0 in 8000 (95% confidence interval 0-3).

Campylobacter Infections↗
PubMed1999

Developmental and pharmacological regulation of apolipoprotein C-II gene expression. Comparison with apo C-I and apo C-III gene regulation.

Increased plasma triglyceride concentrations are often observed in metabolic disorders predisposing to coronary heart disease. Among the major determinants of plasma triglyceride metabolism are the apolipoproteins (apos) of the C class, C-I, C-II, and C-III. Whereas physiological concentrations of apo C-II are required for lipolysis of triglycerides by lipoprotein lipase (LPL), overexpression of all 3 C apolipoproteins leads to hypertriglyceridemia. In the present study, we investigated apo C-II gene regulation under conditions associated with profound changes in plasma triglyceride metabolism, ie, during postnatal development and after treatment with the triglyceride-lowering fibrate drugs, and compared its expression to that of apo C-I and apo C-III. Whereas the expression of both apo C-I and apo C-III is low in fetal liver, increases gradually after birth, and attains maximal levels after weaning, apo C-II gene expression is already detectable in the fetal liver, increases rapidly immediately after birth, and remains elevated throughout suckling. Thus, the increased ingestion of lipids during suckling is met by an earlier induction of apo C-II, the obligatory activator for LPL, compared with apo C-III and apo C-I, which antagonize triglyceride catabolism. Treatment of rats with fibrates decreased apo C-II gene expression in the liver, but not in the intestine, whereas apo C-I gene expression did not change. The decrease of liver apo C-II mRNA levels after fenofibrate occurred in a time- and dose-dependent manner and was reversible but appeared less pronounced than the decrease of apo C-III mRNA. Apo C-II mRNA levels were not affected after treatment with BRL49653, a peroxisome proliferator-activated receptor (PPAR)gamma-specific ligand, suggesting that fibrates act on apo C-II expression via PPARalpha. Addition of fenofibric acid to primary rat and human hepatocytes resulted in a decrease of apo C-II expression. In conclusion, fibrates decrease gene expression of apo C-II and apo C-III, but not apo C-I, in rat and human hepatocytes. This decrease of apo C-II and apo C-III gene expression, together with a lowered apo C-III to apo C-II ratio, should result in an improved clearance of triglyceride-rich remnant lipoproteins from plasma, without hampering triglyceride lipolysis by LPL.

Aging↗
PubMed1998

In vitro and in vivo characterization of (+)-3-[11C]cyano-dizocilpine.

(+)-3-[11C]Cyano-5-methyl-10,11 -dihydro-5H-dibenzo[a,d]-cyclohepten-5,10-imine ([11C]MKC) was successfully synthesized as a potential radiotracer for PET studies on the NMDA receptor channel complex. In vitro binding properties of [11C]MKC were investigated with newly developed techniques for efficient evaluation of 11C-labeled compounds. The association curve of [11C]MKC binding in rat forebrain membranes showed that the specific binding reached an equilibrium within 30 min. Specific binding was saturable with affinity constant KD=8.2+/-0.4nM and Bmax=1.62+/-0.04 pmol/mg protein with glutamate and glycine included in the incubation medium. The binding of [11C]MKC was decreased by extensive washing of the membrane preparation. (+)- and (-)-Dizocilpine, 3-cyano-dizocilpine, and ketamine inhibited the specific binding of [11C]MKC with IC50 values of 37.3, 445.0, 65.8nM and 3.91 microM, respectively. High specific binding in in vitro autoradiography was distributed predominantly in telencephalic regions (the hippocampus, cerebral cortex, and striatum) followed by thalamus. PET studies using rhesus monkeys under anesthesia showed high uptake of [11C]MKC in the temporoparietal and frontal cerebral cortices, striatum, and thalamic regions, although it is problematic to verify the specific binding in vivo by PET.

Animals↗
PubMed1998

Synthesis of 11C/13C-labelled prostacyclins.

A one-pot synthesis of (15R)-16-(3-[11C]methylphenyl)-17,18,19, 20-tetranoriso-carbacyclin methyl ester was performed using a palladium-promoted reaction of [11C]methyl iodide with (15R)-16-(3-tri-n-butylstannylphenyl)-17,18,19, 20-tetranorisocarbacyclin methyl ester. The C-15 epimer (15S)-16-(3-[11C]methylphenyl)-17,18,19,20-tetranorisocarbacyclin methyl ester was synthesised in the same way starting from (15S)-16-(3-tributylstannylphenyl)-17,18,19,20-tetranorisocarba cyclin methyl ester. The decay-corrected radiochemical yields were 33-45% based on [11C]methyl iodide produced, and the radiochemical purity of the product was > 95%. The total synthesis time was 35 min, counted from end of radionuclide production to product ready for administration. The 11C-labelled prostacyclin methyl esters were easily hydrolysed using sodium hydroxide affording the 11C-labelled prostacyclin acids in quantitative yields. The stereoisomers (15R)-16-(3-methylphenyl)-17,18,19,20-tetranorisocarbacyclin [11C]methyl ester and (15S)-16-(3-methylphenyl)-17,18,19,20-tetranorisocarbacyclin [11C]methyl ester were synthesised by esterification using [11C]methyl iodide and the tetrabutylammonium salts of (15R)-16-(3-methylphenyl)-17,18,19,20-tetranorisocarbacyclin acid and (15S)-16-(3-methylphenyl)-17,18,19,20-tetranorisocarbacyclin acid, respectively. The decay-corrected radiochemical yields were in the range of 55% counting from [11C]methyl iodide produced, and the radiochemical purity of the product was > 95%. The total synthesis time was 35 min, counting from end of radionuclide production to product ready for administration. Both of these labelling methods can be used for labelling with 13C when (13C)methyl iodide is used. The methods described herein have already proved important since they enable the in vivo use of PET to study the action of prostacyclins in the brain.

Carbon Isotopes↗
PubMed1997

Methodological aspects for in vitro characterization of receptor binding using 11C-labeled receptor ligands: a detailed study with the benzodiazepine receptor antagonist [11C]Ro 15-1788.

As a complement to in vivo studies with positron emission tomography (PET), it is desirable to perform in vitro characterization of newly developed 11C tracers. In this report we describe the technique for determination of receptor-ligand kinetics utilizing ligands labeled with the short-lived radionuclide 11C. The limitations and advantages are discussed. The benzodiazepine antagonist [11C]Ro 15-1788 was used as a model substance, and the use of storage phosphor plates for quantification of radioactivity was validated. Storage phosphor plates showed an excellent linear range (approximately 10[3]) and acceptable resolution (approximately 0.5 mm). Receptor-ligand kinetics, including depletion, association and dissociation, saturation and displacement were evaluated with good results through the use of short-lived radiotracers and storage phosphor plates.

Animals↗
PubMed1997

Three variants of parathyroid hormone-related protein messenger RNA are expressed in human mammary gland.

PTH-related protein (PTHrP) is found in a variety of tissues; particularly high levels are present in human milk. The structure of the human PTHrP gene is complex, and alternative splicing allows expression of three different variants PTHrP139, PTHrP173, and PTHrP141, respectively. To determine which of the variants are expressed in human mammary gland a reverse transcriptase polymerase chain reaction (RT-PCR) method was elaborated, distinguishing the three variants. mRNA isolated from human milk cells, human mammary epithelial cells (HMEC) and human nonlactating mammary gland cells were analyzed. The RT-PCR experiments resulted in amplification of DNA fragments corresponding to all three variants for all three cell sources tested. The nucleotide sequences of the PCR fragments were determined and verified to be identical to the reported sequences. Hence, it is concluded that human mammary gland epithelial cells express three variants of PTHrP. Whether these have different physiologic effects in the mammary gland or in the breast fed infant remain to be explored.

Adult↗
PubMed1997

Guinea pig apolipoprotein C-II: expression in E. coli, functional studies of recombinant wild-type and mutated variants, and distribution on plasma lipoproteins.

Guinea pig apolipoprotein C-II (apoC-II) lacks four amino acid residues in the amino-terminal, lipid-binding part compared to apoC-II from other mammalian species (Andersson et al. 1991. J. Biol. Chem. 266: 4074-4080). To explore whether this structural difference explains the low ability of guinea pig plasma to activate lipoprotein lipase in vitro, we have expressed guinea pig apoC-II in Escherichia coli and have constructed an insertion mutant with the four missing amino acid residues compared to human apoC-II. With a synthetic emulsion of long-chain triacylglycerols, both the wild-type guinea pig apoC-II and the insertion mutant stimulated lipoprotein lipase similar to human apoC-II, but with chylomicrons from an apoC-II-deficient patient, 5- to 10-fold more of both wild-type guinea pig apoC-II and the insertion mutant were needed. Studies of tryptophane fluorescence indicated a slight difference in how guinea pig apoC-II interacted with liposomes, and presumably with lipoproteins, as compared to human apoC-II. The level of apoC-II (11.5 +/- 5.4 microg/ml) was lower in guinea pig compared to human plasma, and most of guinea pig apoC-II was on HDL-like particles. These had decreased ability to donate apoC-II to lipid emulsions compared to human HDL. Some guinea pig apoC-II was associated with LDL which, as demonstrated by surface plasmon resonance, had higher affinity for lipoprotein lipase than human LDL, and inhibited rather than stimulated the lipase reaction in vitro. We conclude that while guinea pig apoC-II is fully competent to stimulate lipoprotein lipase, the sum of several different factors explains the low ability of guinea pig plasma to accomplish stimulation.

Animals↗
PubMed1996

Apolipoprotein CII from chicken (Gallus domesticus). The amino-terminal domain is different from corresponding domains in mammals.

The amino acid sequence of chicken apolipoprotein CII (apoCII) was determined from cDNA sequencing and from partial protein sequencing. The chicken sequence showed an overall identity of around 30% to all the other previously known apoCII sequences. Comparison of the carboxyl-terminal domain (residues 51-79, human numbering) showed at least 50% identity between species. By limiting the region to residues 51-70 the similarity was remarkably high, about 85%. This is in concert with the previous opinion that residues in the region 56-76 are directly engaged in binding to lipoprotein lipase and in activation of this enzyme. In contrast, in the amino-terminal end up to residue 50 (human numbering) less than 24% of the amino acid residues in chicken apoCII were identical to residues of any of the other species. In addition, chicken apoCII is four residues longer than human apoCII (83 versus 79 residues), probably due to an extension at the amino-terminal end. Although the sequence was completely different in the amino-terminal domain, the structures necessary for binding to lipid appear to be present in chicken apoCII. Secondary structure prediction showed that the amino-terminal domain could form two amphipathic alpha-helices in almost similar areas of the sequence as was previously predicted for human apoCII.

Amino Acid Sequence↗
PubMed1996

Receptor imaging technique with 11C-labeled receptor ligands in living brain slices: its application to time-resolved imaging and saturation analysis of benzodiazepine receptor using [11C]Ro15-1788.

Recently we developed a novel imaging technique using positron emitter-labeled compounds as probes and a storage phosphor screen as a detector. This approach makes it possible to follow a variety of biochemical processes with spatial information in living brain slices. Further technical development is reported here in terms of time-resolved imaging and receptor characterization in a real equilibrium state. The method was validated by use of [11C]Ro15-1788, a benzodiazepine receptor antagonist. Fresh brain slices were incubated with [11C]Ro15-1788 in oxygenated Krebs-Ringer solution at 37 degrees C, in a specially designed chamber. By placing the chamber on a storage phosphor screen, we could obtain two-dimensional images of radioactivity in the slices. Time-resolved imaging was made at 5 min intervals, revealing that it took 60 min to reach equilibrium binding. The dissociation process was observed by adding an excess amount of unlabeled Ro15-1788 to the chamber, 25 min was required for the full dissociation. In the equilibrium state, i.e. in the presence of free radio-ligand, Scatchard plot analysis was performed on the cerebral cortex (Kd = 7.4 nM, Bmax = 146 fmol/mg tissue) and striatum (Kd = 7.5 nM, Bmax = 107 fmol/mg tissue), suggesting the presence of a single component of binding site in these two regions. The present method, for the first time, made it possible to study a ligand-receptor interaction in living brain slices with temporal and spatial resolutions. This technique should prove useful for studies of receptor function under physiological conditions.

Animals↗
PubMed1995

Neurological Wilson's disease studied with magnetic resonance imaging and with positron emission tomography using dopaminergic markers.

Four patients with neurological Wilson's disease were investigated using magnetic resonance imaging (MRI) and positron emission tomography (PET). All patients had dystonia as their major clinical manifestation but also had dysarthria and at the presentation of the disease had choreoathetoid movements in at least one limb. A multitracer approach with PET was used to visualize various aspects of dopaminergic function; [11C]-(+)-nomifensine (NMF), [11C]raclopride (RAC) and [11C]-L-DOPA (one patient). Correlation analysis of RAC and NMF binding as well as putamen/caudate uptake ratios showed corresponding reductions. The patient investigated with [11C]-L-DOPA had a normal striatal uptake. Generally, structural changes as shown by MRI corresponded to reductions both in NMF and RAC binding. There was no evident correspondence between PET findings and the severity of clinical symptoms seen in the individual patient. In two patients with discrete neurological impairment at the time of investigation, PET showed serious presynaptic dopaminergic lesions in the putamen. Our data suggest that the striatal degeneration seen in Wilson's disease comprises a complex pathology involving both afferent and efferent projections. The discrete neurological impairment seen in some patients with gross striatal pathology might be due to concomitant lesions in functionally counteracting basal ganglia circuits.

Adult↗
PubMed1995

Outbreak of Shigella sonnei infection traced to imported iceberg lettuce.

In the period from May through June 1994, an increase in the number of domestic cases of Shigella sonnei infection was detected in several European countries, including Norway, Sweden, and the United Kingdom. In all three countries epidemiological evidence incriminated imported iceberg lettuce of Spanish origin as the vehicle of transmission. The outbreaks shared a number of common features: a predominance of adults among the case patients, the presence of double infections with other enteropathogens, and the finding of two dominant phage types among the bacterial isolates. In Norway 110 culture-confirmed cases of infection were recorded; more than two-thirds (73%) were adults aged 30 to 60 years. A nationwide case-control study comprising 47 case patients and 155 matched control individuals showed that the consumption of imported iceberg lettuce was independently associated with an increased risk of shigellosis. Epidemiological investigation of a local outbreak incriminated iceberg lettuce from Spain, consumed from a salad bar, as the source. The presence of shigellae in the suspected food source could not be documented retrospectively. However, high numbers of fecal coliforms were detected in iceberg lettuce from patients' homes. Three lettuce specimens yielded salmonellae. The imported iceberg lettuce harbored Escherichia coli strains showing resistance to several antimicrobial agents, including ampicillin, ciprofloxacin, gentamicin, and trimethoprim-sulfamethoxazole. During the outbreak it is likely that thousands of Norwegians and an unknown number of consumers in other countries were exposed to coliforms containing antibiotic resistance genes.

Adolescent↗
PubMed1994

Synthesis of 11C-labelled benzamide compounds as potential tracers for poly(ADP-ribose) synthetase.

Poly(ADP-ribose) synthetase catalyses the synthesis of poly(ADP-ribose) from NAD+, thereby releasing the DNA from histones to a transcriptionally and reparationally active form. In order to investigate if in vivo and in vitro studies of this enzyme are feasible to perform with PET, the poly(ADP-ribose) synthetase inhibitors benzamide, 3-aminobenzamide, 3-methoxybenzamide and nicotinamide were labelled with carbon-11 in the amide group. Starting with the corresponding aromatic halides and hydrogen [11C]cyanide, the substituted [11C]benzonitriles were prepared using a palladium promoted reaction. Conversion of the nitriles to [carboxy-11C]amides was achieved by reaction with sodium percarbonate. A one-pot procedure for the synthesis of the 11C-labelled aromatic amides was developed. The total synthesis time including reversed-phase HPLC purification was 25-35 min. Decay-corrected radiochemical yield was 45-70% and the radiochemical purity > 99%. The specific radioactivity was in the order of 2-3 Ci.mumol-1. Initial distribution and kinetic studies were performed in monkey using the tracer substance injected as a rapid bolus. These studies demonstrated that the blood-clearance was fast for [carboxy-11C]nicotinamide but considerably slower for 3-amino[carboxy-11C]benzamide and 3-methoxy[carboxy-11C]benzamide. The brain uptake was low for all substances except 3-methoxy[carboxy-11C]benzamide which initially had a high brain uptake, followed by a rapid wash-out. The 11C-labelled nicotinamide demonstrated a rapid fixation with high uptake values in the liver, kidney and lymph nodes.

Animals↗
PubMed1992

Brain kinetics of 11 C-labelled L-tryptophan and 5-hydroxy-L-tryptophan in the rhesus monkey. A study using positron emission tomography.

5-Hydroxy-L-tryptophan labelled with 11 C is introduced as a tracer for the in vivo assessment of brain serotonin synthesis in the Rhesus monkey using positron emission tomography, PET. Increasing radioactivities were seen in the striatal area in contrast to that seen in other brain regions. Following 11 C-labelled L-tryptophan an even spread of brain radioactivity was seen. This selective increase most probably results from the decarboxylation of tracer and retention of formed products since no striatal increase of radioactivity was seen when 5-hydroxy-L-tryptophan labelled with 11 C in the carboxy-position was administered. Furthermore, pretreatment of the monkey with a centrally active decarboxylase inhibitor (NSD 1015, 10 mg/kg) did not lead to increased striatal radioactivities after the administration of 5-hydroxy-(beta-11 C)-L-tryptophan. The selective utilization of the radiotracer in the striatal area increased with a rate constant calculated to be 0.0055 +/- 0.0015 min-1 (n = 5) using the surrounding brain as reference area. A non-significant influence of radiolabelled metabolites to the rate constants measured was shown after pretreatment of the monkeys with selective and non-selective monoamine oxidase inhibitors, respectively. These results may give a basis for the use of the new tracer 5-hydroxy-(beta-11 C)-L-tryptophan in PET-studies of brain serotonin metabolism in health and disease.

5-Hydroxytryptophan↗