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Biomedical subjects

H Nissen

Publications and source records attributed to H Nissen.

At least 19 recordsLinked to original sources
PubMed2002

Safety evaluation of sous vide-processed ready meals.

AIMS: To assess survival, growth and toxin production of spore-forming bacteria in sous vide products exposed to a relatively high heat treatment. METHODS AND RESULTS: During a three-year period, 2,168 sous vide-processed, commercially available ready-made meals with a shelf life of 3-5 weeks were examined. The products were stored at 4 degrees C for the first 1/3 and at 7 degrees C for the remaining 2/3 of their shelf life period. Three-fourths of the samples had less than 10 bacteria per gram the day after production, and none had more than 1,000. Similar numbers were found at the end of the shelf life when stored as described above. At abuse temperature (20 degrees C), the number of bacteria increased to 10(6)-10(7) cfu g(-1) 7 d after production. A total of 350 isolates of Bacillus spp. were collected, but no Clostridium strains were detected. Only 11 of the 113 tested strains were able to grow at 7 degrees C in broth, and none of the psychrotrophic strains were able to produce substantial amounts of toxins causing food poisoning. CONCLUSION: The health risk of these products is small as long as the temperature during storage is low. For microbial testing of the end products, traditional plating will suffice.

Animals↗
PubMed2001

Identification of recurrent and novel mutations in the LDL receptor gene in German patients with familial hypercholesterolemia.

In order to identify mutations in the low density lipoprotein receptor (LDLR) gene in primary hypercholesterolemia, we screened 100 unrelated German individuals with elevated plasma LDL-C (LDL-C > 4,7 mmol/l) for mutations in the 18 exons and their flanking intronic sequences including the promoter region of the LDL-R gene using a combination of polymerase chain reaction (PCR), denaturing gradient gel electrophoresis (DGGE) and direct sequencing. In addition we tested all patients for the presence of mutations in codons 3456 - 3553 of the gene encoding apolipoprotein B-100. In 56 individuals we detected 37 different mutations affecting the LDL-R gene, 16 of which, designated C122R, C127Y, C163W, F179L, R236W, E296X, R553C, V618D, T721I, V785D, G1358+2A, 257delTCTGGAGGT, 657delC, 676insACGGTATGGACTGCAdelGACG, C1205delTCT, 2420delTCCTTCT, have not yet been reported. One proband was a compound heterozygote showing two separate sequence variations (E207X and T705I). Seven patients were heterozygous for the mutation R3500Q within the apoB-100 gene. These results demonstrate that there is a broad spectrum of mutations in the LDL-R gene and that the R3500Q mutation is a frequent cause of hypercholesterolemia in the German population.

Adolescent↗
PubMed2001

Characterization, production, and purification of carnocin H, a bacteriocin produced by Carnobacterium 377.

Carnocin H, a bacteriocin produced by a Carnobacterium sp., inhibited lactic acid bacteria, clostridia, enterococci, and some Staphylococcus aureus strains. Some strains of Listeria and Pediococcus were also sensitive to carnocin H. The bacteriocin was produced during the late stationary growth phase. Carnocin H was purified by cation exchange chromatography and reverse phase chromatography. Amino acid sequence and composition indicate that carnocin H is a novel bacteriocin belonging to the class II bacteriocins. The bacteriocin consists of approximately 75 amino acid residues with a highly cationic N-terminal containing six succeeding lysines. Activity, as measured by agar diffusion zones, was reduced at increased pH values, levels of indicator bacteria, NaCl, agar, and soy oil.

Amino Acid Sequence↗
PubMed2001

Measurements of nitrogen dioxide in Greenland using Palmes diffusion tubes.

Measurements of nitrogen dioxide using the Palmes diffusion tubes in Uummannaq, Aasiaat, and Nuuk. all located along the west-coast of Greenland, have demonstrated that the levels of pollution at the most heavily impacted sites are comparable to levels in much larger towns in Denmark. The highest concentrations were, in general, observed near sites influenced by car traffic (peak concentrations of up to 16 ppbv), medium concentrations were observed in the residential areas (2 6 ppbv), and very low levels were found at the background locations in the town outskirts (1-2 ppbv). Observations of nitrogen dioxide concentrations less than 0.1 ppbv at a remote site, Akia, 25 km from Nuuk, indicate that, compared to local sources, long-range transport of nitrogen dioxide is not important in western Greenland.

Air Pollution↗
PubMed2001

Characterization and growth of Bacillus spp. in heat-treated cream with and without nisin.

AIMS: To study the germination and growth of both inoculated and naturally occurring Bacillus strains in heat-treated cream with and without nisin. METHODS AND RESULTS: In heat-treated cream (90 degrees C for 15 min) stored at 8 degrees C, growth was dominated by naturally occurring Bacillus strains such as Bacillus pumilus and B. licheniformis. Only six of the 52 isolated strains were B. cereus/thuringiensis. All of the B. cereus strains, but none of the other strains, produced enterotoxin when tested with the TECRA and reverse passive latex agglutination kits. Bacterial growth during storage of the cream at 8 or 10 degrees C was completely inhibited by low concentrations of nisin. CONCLUSION: The high number of Bacillus strains surviving the heat treatment represent a risk for heat-treated food that contains cream. The safety of the cream, for instance in "ready-to-eat" products, can be improved by the addition of low concentrations of nisin. SIGNIFICANCE AND IMPACT OF THE STUDY: Spores of several Bacillus species may survive heat treatment of cream, but low concentration of nisin with inhibit germination and growth.

Anti-Bacterial Agents↗
PubMed2001

Familial hypercholesterolaemia in Finland: common, rare and mild mutations of the LDL receptor and their clinical consequences. Finnish FH-group.

Familial hypercholesterolaemia (FH) is an autosomal co-dominantly inherited condition resulting from mutations of the low-density lipoprotein (LDL) receptor which occur in heterozygous form in approximately one in 500 individuals. Clinically, FH is characterized by 2-3-fold elevation of serum LDL cholesterol levels, accelerated development of atherosclerotic vascular disease, and, if untreated, shortened lifespan. The Finnish population, which represents a genetic isolate, offers exceptional possibilities for genetic-epidemiological studies on FH, as a handful of founder gene mutations account for the majority of FH cases in Finland. This review summarizes data from our FH studies carried out since 1985. We wish to emphasize the continuum of genotype-phenotype relationships, the importance of molecular diagnosis, the detection of novel risk factors of vascular disease, and innovations inhibiting cholesterol absorption for the modern treatment of FH.

Age of Onset↗
PubMed2000

Comparison between the growth of Yersinia enterocolitica, listeria monocytogenes, escherichia coli O157:H7 and salmonella spp. in ground beef packed by three commercially used packaging techniques.

Growth of the pathogens Yersinia enterocolitica, Listeria monocytogenes, Escherichia coli O157:H7 and strains of Salmonella were compared in ground beef packed in modified atmospheres of 60% CO2/40% N2/0.4% CO (high CO2/low CO mixture), 70% O2/30% CO2 (high O2 mixture) and in chub packs (stuffed in plastic casings). The ground beef was inoculated with rifampicin-resistant or nalidixic acid/streptomycin-resistant strains of the pathogens (final concentration 10(2) - 10(3) bacteria/g) and stored at 4 and 10 degrees C for up to 14 days. At 4 degrees C the shelf life, based on colour stability and background flora development, was prolonged for the high CO2/low CO mixture compared to the two other packaging methods, but at 10 degrees C the shelf life was < 8 days for all the packaging methods. Growth of Y. enterocolitica was nearly totally inhibited both at 4 and 10 degrees C in the high CO2/low CO mixture, while the bacterial numbers in the samples packed in the high O2 mixture increased from about 5 x 10(2) bacteria/g at day 0 to about 10(4) at day 5 at 4 degrees C and to 10(5) at 10 degrees C. Growth in the chub packs was even higher. L. monocytogenes showed very little growth at 4 degrees C in all treatments. At 10 degrees C there was slow growth from about 5 x 10(3) bacteria/g to about 10(4) at day 5 in the high CO2/low CO mixture, while the numbers in the high O2 mixture and the chub packs were about 10 times higher. Growth of E. coli O157:H7 at 10 degrees C in the ground beef was nearly totally inhibited in both the high CO2/low CO mixture and the high O2 mixture. Growth in the chub packs was higher, as the number of bacteria increased 3 log in 5 days. The Salmonella strains (S. typhimurium, S. dublin, S. enteritidis and S. enterica 61:k:1,5,(7)) in the ground beef stored at 10 degrees C for 5 and 7 days grew to a higher number in the high CO2/low CO mixture than in the high O2 mixture. This study shows that the growth of Y. enterocolitica and L. mononcytogenes in ground beef stored in the high CO2 /low CO mixture was not increased as a result of prolonging the shelf life. However, the observed growth of strains of Salmonella at 10 degrees C in this mixture and in chub packs does emphasise the importance of temperature control during storage.

Animals↗
PubMed2000

High levels of background flora inhibits growth of Escherichia coli O157:H7 in ground beef.

The influence of natural background flora under aerobic and anaerobic incubation on the growth of Escherichia coli O157:H7 in ground beef was investigated. The background flora from eight different commercial ground beef were added to ground beef spiked with E. coli O157:H7 and stored either aerobically or anaerobically at 12 degrees C. The results showed that the presence of a large number of background bacteria in the ground meat inhibited the growth of E. coli O157:H7 both aerobically and anaerobically. Inhibition was more pronounced under anaerobic conditions. The background floras consisted mainly of lactic acid bacteria of which approximately 80% were Lactobacillus sakei. These results show the importance of the natural background flora in meat for inhibition of growth of E. coli O157:H7.

Aerobiosis↗
PubMed2000

FH-Freiburg: a novel missense mutation (C317Y) in growth factor repeat A of the low density lipoprotein receptor gene in a German patient with homozygous familial hypercholesterolemia.

We describe the characterization of a novel mutation in the low density lipoprotein receptor (LDL-R) gene in a patient with true homozygous familial hypercholesterolemia (FH). The combined use of denaturing gradient gel electrophoresis (DGGE) and sequencing of genomic DNA revealed a guanine to adenine base substitution at nucleotide position 1013 of the LDL-R cDNA. This point mutation results in a change from cysteine to tyrosine at amino acid residue 317 of repeat A of the epidermal growth factor (EGF) precursor homology domain. Binding, uptake and degradation of iodinated LDL in skin fibroblasts from the homozygous patient were less than 10% of normal. In contrast, binding, uptake and degradation of iodinated VLDL was reduced by only 60, 30, and 38%, respectively. Incubation of the patient's fibroblasts in the presence of cholesterol diminished the residual binding of VLDL by 50%, suggesting that the loss of the highly conserved cysteine at position 317 results in a LDL-R that fails to bind LDL, but retains some ability to bind VLDL by interacting with the apolipoprotein E. Both parents were heterozygous for the C317Y mutation. Interestingly, however, the father presented with markedly elevated levels of triglycerides and VLDL cholesterol, whereas his LDL cholesterol was unexpectedly low. The mother of the index patient had only slightly elevated LDL cholesterol. These observations testify to the biological complexity of genotype-environment interactions in individuals carrying mutations at the LDL-R locus and indicate that genetic analysis importantly complements the clinical and biochemical diagnosis of patients with hyperlipidemia.

Adolescent↗
PubMed2000

Predominance of a 6 bp deletion in exon 2 of the LDL receptor gene in Africans with familial hypercholesterolaemia.

In South Africa, the high prevalence of familial hypercholesterolaemia (FH) among Afrikaners, Jews, and Indians as a result of founder genes is in striking contrast to its reported virtual absence in the black population in general. In this study, the molecular basis of primary hypercholesterolaemia was studied in 16 Africans diagnosed with FH. DNA analysis using three screening methods resulted in the identification of seven different mutations in the coding region of the low density lipoprotein (LDLR) gene in 10 of the patients analysed. These included a 6 bp deletion (GCGATG) accounting for 28% of defective alleles, and six point mutations (D151H, R232W, R385Q, E387K, P678L, and R793Q) detected in single families. The Sotho patient with missense mutation R232W was also heterozygous for a de novo splicing defect 313+1G-->A. Several silent mutations/polymorphisms were detected in the LDLR and apolipoprotein B genes, including a base change (g-->t) at nucleotide position -175 in the FP2 LDLR regulatory element. This promoter variant was detected at a significantly higher (p<0.05) frequency in FH patients compared to controls and occurred in cis with mutation E387K in one family. Analysis of four intragenic LDLR gene polymorphisms showed that the same chromosomal background was identified at this locus in the four FH patients with the 6 bp deletion. Detection of the 6 bp deletion in Xhosa, Pedi, and Tswana FH patients suggests that it is an ancient mutation predating tribal separation approximately 3000 years ago.

Adolescent↗
PubMed1998

Evaluation of a clinically applicable mutation screening technique for genetic diagnosis of familial hypercholesterolemia and familial defective apolipoprotein B.

We have recently developed a simple mutation screening assay based on the denaturing gradient gel electrophoresis (DGGE) technique for detection of mutations in the coding and regulatory regions of the low density lipoprotein receptor (LDLR) gene and the codon 3500 region of the apolipoprotein (apo) B-100 gene leading to familial hypercholesterolemia (FH) and familial defective apo B-100 (FDB), respectively. To evaluate the assay, 14 Danish families suspected of FH were studied. In ten families, the DGGE assay detected seven different point mutations, including mutations undescribed prior to establishing the assay. In addition, in one of these ten families and in one of the remaining four families, Southern blotting detected the FH-DK3 exon 5 deletion. Based on segregation analysis and clinical data, the FH diagnosis was dubious in the remaining three families without DGGE or Southern blotting detectable mutations. In conclusion, a simple DGGE based mutation screening assay may detect underlying mutations in most FH/FDB families, thus allowing its routine use in genetic counselling of FH-families.

Animals↗
PubMed1998

Mutation screening of the LDLR gene and ApoB gene in patients with a phenotype of familial hypercholesterolemia and normal values in a functional LDL receptor/apolipoprotein B assay.

Mutations in the LDL receptor (LDLR) or the apolipoprotein B-100 genes causing familial hypercholesterolemia (FH) and familial defective apolipoprotein B-100 (FDB), two of the most frequent inherited diseases, are the underlying genetic defects in a small proportion of patients suffering from premature atherosclerotic heart disease. Consequently, secure diagnostic tools for these conditions allowing early preventive measures are needed. Since clinical and biochemical diagnosis often is inaccurate, assays analyzing patient LDLR function and LDL affinity have been established. These assays are, however, not able clearly to differentiate between suspected FH/FDB samples and normal controls. To evaluate if this may be caused by other hitherto undescribed genetic defects or to failure of the functional assays, we undertook denaturing gradient gel electrophoresis based mutation screening of the LDLR gene and the codon 3456 3553 region of the apolipoprotein B gene in six French FH/FDB patients with normal outcomes on functional assays. In all six patients, pathogenic LDLR mutations were found, including three previously undescribed mutations, suggesting that failure of the functional assays explains the normal results found in some phenotypic FH/FDB patients and illustrating the need for DNA based screening techniques for routine genetic diagnosis in FH/FDB.

Apolipoprotein B-100↗
PubMed1998

Detection of mutations in the apolipoprotein CII gene by denaturing gradient gel electrophoresis. Identification of the splice site variant apolipoprotein CII-Hamburg in a patient with severe hypertriglyceridemia.

Familial apolipoprotein (apo) CII deficiency is a rare autosomal recessive inborn error of metabolism clinically resembling lipoprotein lipase deficiency. A number of mutations of the apo CII gene are known to date; they are located in the promoter region, the coding exons, or in the splice junctions. We present a simple assay based on PCR and denaturing gradient gel electrophoresis, which allows scanning of the promoter, the entire coding sequence, and the splice junctions of the apo CII gene for sequence variants. All gene fragments are amplified using a common PCR protocol and are examined for mutations on a single gradient gel. Using this method and direct sequencing, we identified homozygosity for a donor splice-site mutation in the second intron, previously designated apo CII-Hamburg, as the genetic cause of apo CII deficiency in a 9-year-old boy presenting with chylomicronemia, eruptive xanthoma, and pancreatitis. In addition, the method allowed us to detect all of six different other known mutations of the apo CII gene. We conclude, therefore, that our assay is highly sensitive; in addition, it is easy to perform and may facilitate the differential diagnosis of disorders of lipoprotein metabolism at the genetic level.

Alternative Splicing↗
PubMed1997

Addition of 2.5% lactate and 0.25% acetate controls growth of Listeria monocytogenes in vacuum-packed, sensory-acceptable servelat sausage and cooked ham stored at 4 degrees C.

A study of the inhibitory effects of propylparaben and of a combination of lactate and acetate against growth of Listeria monocytogenes in inoculated liquid medium, sliced servelat sausage and cooked ham, were performed using rifampicin resistant Listeria strains in inoculation experiments. A consumer acceptance test of products produced with and without the compounds was also performed. Propylparaben was found to be effective in a model liquid non-fat medium, but was without effect in the actual products. This illustrates the potential pitfalls in translating results from studies in liquid media to fat-containing food products. The combined inhibitory and sensory results showed that a mixture of 2.5% lactate and 0.25% acetate (w/w, calculated on the water phase), could be used to increase the margins of safety for sliced and spreadable vacuum-packed ready-to-eat cooked meat products stored for 4-6 weeks. In addition, strict control of temperature during production and storage is very important.

Acetic Acid↗
PubMed1997

Detection and characterization of a novel splice mutation in the LDL receptor intron 12 resulting in two different mutant mRNA variants.

Using a simple, standardized denaturing gradient gel electrophoresis (DGGE) based mutation screening technique, a novel G-to-A mutation in the last base of the intron 12 splice acceptor site of the LDL receptor gene was found in 2 Danish families with familial hypercholesterolemia (FH). The mutation is shown to result in 2 mRNA splice variants, both leading to truncated LDLR proteins, containing only the first 594 of the normal 839 amino acids. In one of the FH-families harbouring the mutation, a striking difference in the clinical picture amongst biochemically diagnosed FH patients was clarified when genetic analysis showed that 2 hypercholesterolemic family members, who despite advanced age had no atherosclerotic disease, had not inherited the family LDLR mutation. DGGE analyses of the LDLR exons, LDLR promoter, and apolipoprotein B codon 3456-3553 as well as Southern blotting of the LDLR gene were without signs of other mutations in the non-atherosclerotic hypercholesterolemics of the family. Availability of the clinically applicable mutation screening assay for FH may thus aid in defining reasons for phenotypic differences in FH families and potentially supply information allowing a more differentiated therapeutic approach to individual members of FH families.

Adolescent↗
PubMed1997

Common founder mutation in the LDL receptor gene causing familial hypercholesterolaemia in the Icelandic population.

Haplotype analysis in 18 apparently unrelated families with familial hypercholesterolaemia (FH) in Iceland has identified at least five different chromosomes cosegregating with hypercholesterolaemia. The most common haplotype was identified in 11 of the 18 families, indicating a responsible for FH in the Icelandic population. By using single-strand conformation polymorphism (SSCP) and direct sequencing of amplified DNA, we identified a novel mutation (a T to a C) in the second nucleotide in the 5' part of intron 4 in the LDL receptor gene. This mutation was present in approximately 60% of the FH families (10/18), supporting the prediction of a common founder. These families could be traced to a common ancestor in half of the cases by going back no further than the eighteenth century. The mutation was predicted to affect correct splicing of exon 4, and analysis at the cellular level demonstrated an abnormal mRNA containing intron 4 sequence in lymphoblastoid cells from a patient carrying this mutation. Translation of the mRNA would lead to a premature stop codon and a truncated nonfunctional protein of 285 amino acids. The novel sequence change created a new restriction site for the restriction endonuclease NlaIII, and using this assay, 29 unrelated individuals with possible FH attending a lipid clinic for treatment were examined for this mutation. Two individuals in this group of patients were found to be carriers of this mutation, supporting the suggestion of a founder mutation. Using this assay for the detection of FH in the Icelandic population should identify > 60% of these individuals.

Cells, Cultured↗