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Biomedical subjects

A M Vogel

Publications and source records attributed to A M Vogel.

At least 19 recordsLinked to original sources
PubMed2002

Palivizumab prophylaxis of respiratory syncytial virus infection in high-risk infants.

Palivizumab prophylaxis significantly reduces hospitalization for respiratory syncytial virus (RSV) disease in preterm infants. However, palivizumab is very expensive. Data from a New Zealand cost-effectiveness analysis were considered by representatives of the Infectious Diseases and Immunisation, Fetus and Newborn, and Respiratory Committees of the Paediatric Society of New Zealand. Prophylaxis in all high-risk groups was associated with net cost. The consensus panel recommends that the priority for palivizumab be given to babies discharged on home oxygen with chronic lung disease, followed by babies born at 28 weeks or less gestation.

Antibodies, Monoclonal↗
PubMed2002

Cost-effectiveness of palivizumab in New Zealand.

OBJECTIVE: To establish the preterm infant hospitalization risks from respiratory syncytial virus (RSV) in New Zealand and the net cost per hospitalization averted by palivizumab. METHODS: The 437 infants born < 32 weeks' gestation in 1997 and treated at five major neonatal units were identified. Subsequent admissions during the next 2 years for bronchiolitis, pneumonia and croup were tracked, and information collected on RSV tests performed. Data on the length of stay and hospital costs were used to calculate the potential net cost per hospitalization averted associated with the use of palivizumab and the number needed to treat (NNT) to prevent one hospitalization. RESULTS: Estimated RSV readmission risk before 1 year corrected age in infants < 32 weeks' gestation discharged home on oxygen, and those " 28 weeks' gestation, or between 29 and 31 weeks' gestation with or without chronic lung disease was 42%, 23%, 19%, 10% and 8%, respectively. The NNT with palivizumab to prevent one hospitalization ranged from six to 26 across subgroups. Mean (range) net cost per hospitalization averted was 60,000 New Zealand dollars ($28,000-$166,700). In no subgroup would prophylaxis result in net cost saving. Prophylaxis for all NZ infants " 28 weeks' gestation would cost approximately $1,090,000 net and prevent 29 hospitalizations annually, being equivalent to $37,000 net per hospitalization averted, with eight infants treated to prevent one hospitalization. Alternative assumptions about cost and efficacy failed to alter these findings. CONCLUSION: If value is placed on preventing morbidity, the priority groups for palivizumab prophylaxis are preterm infants discharged home on oxygen, followed by preterm infants of 28 weeks' gestation or less.

Antibodies, Monoclonal↗
PubMed2001

The impact of pacifier use on breastfeeding: a prospective cohort study.

OBJECTIVES: To determine the predictors of pacifier use during the first year of life and to assess the influence of pacifier use on the duration of breastfeeding. METHODOLOGY: A prospective cohort study was conducted. Three hundred and fifty mother-infant pairs were followed to 1 year of age to determine the impact of the use of a pacifier on the duration of breastfeeding. RESULTS: A cohort of 441 mothers were enrolled and 79% participated. Ninety four per cent were followed up to 1 year. Daily pacifier use was associated with early cessation of breastfeeding (risk ratio (RR) 1.71; 95% confidence interval (95%CI) 1.29, 2.28) and a reduced duration of full breastfeeding (adjusted (adj.) RR 1.35; 95%CI 1.05, 1.74). Finger sucking was not associated with a reduced duration of breastfeeding (RR 1.05; 95%CI 0.81, 1.37). Pacifier use less than daily was not associated with a change in duration of breastfeeding (RR 1.02; 95%CI 0.75, 1.39). Most mothers commenced the use of a pacifier within the first month. Multiple logistic regression analysis found that the use of a pacifier was associated with male gender (adj. RR 1.97; 95%CI 1.23, 3.13), maternal smoking in pregnancy (adj. RR 2.23; 95%CI 1.01, 4.95), and low maternal confidence with breastfeeding (adj. RR 2.70; 95%CI 1.48, 4.93). CONCLUSIONS: Daily pacifier use is associated with a reduced duration of breastfeeding. Less frequent pacifier use does not reduce the duration of breastfeeding.

Adult↗
PubMed2000

Isolation, characterization, expression and functional analysis of the zebrafish ortholog of MEN1.

Mutations in the MEN1 gene lead to an autosomal dominant disorder, multiple endocrine neoplasia type 1 (MEN1), which is characterized by tumors of the parathyroid, entero-pancreatic neuroendocrine, and pituitary tissues. The protein encoded by MEN1, 610-amino acid menin, resides primarily in the nucleus and binds to the transcription factor JunD, resulting in the repression of JunD-induced transcription. We report here a detailed characterization of the zebrafish men1 gene and its full-length (2551 nt) transcript, encoding a 617-amino acid protein with 67% identity and 80% similarity to human menin. Of the 81 missense mutations and in-frame deletions reported in MEN1 patients, 72 occur in residues that are identical in zebrafish, suggesting the importance of the conserved regions. The zebrafish men1 gene maps 61 cM from the top of linkage group 7 (LG7), a region that appears to show conserved synteny to the MEN1 loci at human 11q13. A 2.7-kb men1 message is detected at all stages of zebrafish development analyzed, from one-cell embryos to adult fish. Whole-mount in situ hybridization showed ubiquitous distribution of men1 message in zebrafish embryos at cleavage, blastula, gastrula, and early segmentation stages, with relatively abundant expression in blood cell progenitors (24 h post fertilization) and mesenchymal tissues (48 h post fertilization) at later stages. Zebrafish menin binds both human and mouse JunD, and represses JunD-induced transcription, indicating that the JunD-binding ability of menin is evolutionarily conserved.

Amino Acid Sequence↗
PubMed2000

Studying vascular development in the zebrafish.

The zebrafish, a genetically accessible vertebrate with an externally developing, optically clear embryo, is ideally suited for in vivo functional dissection of the embryonic development of the circulatory system. Here, we review the advantages of the zebrafish as a model system for studying vascular development, and describe genetic and experimental tools, methods and resources that have been developed to exploit these advantages. We also discuss briefly how some of these tools and methods can be brought to bear on problems of relevance to human health.

Animals↗
PubMed1999

A zebrafish homolog of the serum response factor gene is highly expressed in differentiating embryonic myocytes.

Serum response factor (SRF) was identified as an activity binding upon serum stimulation of HeLa cells to a motif known as the serum response element in the c-fos promoter. This element is also found in the regulatory regions of many muscle-specific genes. We have characterized srf expression during early zebrafish embryogenesis. In addition to low-level expression in many or even all cells, elevated levels of srf RNA and protein are transiently expressed in skeletal muscle lineages during their differentiation.

Amino Acid Sequence↗
PubMed1999

Promoter activity of the zebrafish bhikhari retroelement requires an intact activin signaling pathway.

We have investigated mesoderm induction in zebrafish employing the zebrafish LTR-retroelement bhikhari (bik). bik elements are transcribed in all early mesendodermal cells. This expression pattern is generated by a promoter located in the U3 region of the LTR. We show that bik is activated through the activin/Vg1 signaling pathway in an immediate early fashion. This activation critically depends on a sequence motif that occurs among others also in the Xenopus Mix2 activin response element (ARE). It has been shown that the Mix2 ARE binds FAST- 1, which complexes with Smad proteins to form a multi-protein complex. We confirm that also the bik ARE can be bound by FAST-1 in vitro. In animal cap experiments we demonstrate that this binding site is required for activin-induced transcriptional activation mediated by FAST and Smad-type proteins.

Activins↗
PubMed1998

The establishment and duration of breastfeeding. Part 1: Hospital influences.

Most New Zealand mothers initiate breastfeeding in hospital, but many continue for only a relatively short time. Focus group discussions with mothers and health care workers on their perceptions of important factors influencing the duration of breastfeeding indicated many negative initial hospital experiences. Specific concerns included overworked staff; lack of health care workers' skills, particularly in helping infants to latch on; inconsistent advice; noise and embarrassment in four bedded rooms; and the impact of changes in the provision of maternity services and funding.

Breast Feeding↗
PubMed1998

The establishment and duration of breastfeeding. Part 2: Community influences.

Most New Zealand mothers initiate breastfeeding in hospital, but many continue for only a relatively short time. This paper reports on mothers' and health care workers' perceptions of important community factors influencing the duration of breastfeeding. Data collection was by focus group discussions. The results indicate that some mothers have specific plans regarding the duration of breastfeeding but many do not. The importance of practical help, realistic role expectations, community acceptance especially amongst men, adequate maternity leave, and help for those returning to work is emphasised. Conflicting opinions exist about the difficulties of introducing older infants to bottles.

Attitude↗
PubMed1996

Prevalence and impact of chronic childhood conditions in Auckland, New Zealand.

OBJECTIVE: To establish the prevalence of specific chronic conditions of childhood in the Auckland area and to quantify resource use by these children. METHODOLOGY: Estimates were made from available registry data and published data sources of the population of children with selected chronic conditions resident in the Auckland Area Health Board area. Resource use data were extracted for admissions to Auckland public hospitals and from providers of community based technology services. RESULTS: The largest community prevalence groups are those with asthma, intellectual handicap, congenital heart disease and epilepsy. Children aged 0-14 with chronic conditions accounted for at least 14,340 hospital days stay in Auckland in 1992 at an estimated minimum cost of $7.9 million. Over 200 children are dependent on technological aids at home. CONCLUSIONS: There are sparse data on the numbers and needs of children with chronic conditions in the population. A non-categorical approach which crosses disease entities may be the best method of meeting common needs.

Child↗
PubMed1995

Mutational analysis of a conserved motif of Agrobacterium tumefaciens VirD2.

The VirD2 polypeptide from Agrobacterium tumefaciens, in the presence of VirD1, introduces a site- and strand-specific nick at the T-DNA borders. A similar reaction at the origin of transfer (oriT) of plasmids is essential for plasmid transfer by bacterial conjugation. A comparison of protein sequences of VirD2 and its functional homologs in bacterial conjugation and in rolling circle replication revealed that they share a conserved 14 residue segment, HxDxxx(P/u)HuHuuux [residues 126-139 of VirD2; Ilyina, T.V. and Koonin, E.V. (1992) Nucleic Acids Res. 20, 3279-3285]. A mutational approach was used to test the role of these residues in the endonuclease activity of VirD2. The results demonstrated that the two invariant histidine residues (H133 and H135) are essential for activity. Mutations at three sites, histidine 126, aspartic acid 128 and aspartic acid 130, that are conserved in a subfamily of the plasmid mobilization proteins, led to the loss of VirD2 activity. Aspartic acid at position 130, could be substituted with glutamic acid and to a much lesser extent, with tyrosine. In contrast, another conserved residue, asparagine 139, tolerated many different amino acid substitutions. The non-conserved residues, arginine 129, proline 132 and leucine 134, were also found to be important for function. Isolation of null mutations that map throughout this conserved domain confirm the hypothesis that this region is essential for function.

Agrobacterium tumefaciens↗
PubMed1994

Molecular characterization of the melanocyte lineage-specific antigen gp100.

The glycoproteins recognized by monoclonal antibody (mAb) NKI-beteb are among the best diagnostic markers for human melanoma because their expression is restricted to melanocytic cells. Recently, we isolated a cDNA clone, termed gp100-c1, which confers immunoreactivity not only to mAb NKI-beteb, but also to two other mAbs used to diagnose malignant melanoma, HMB-50 and HMB-45. In this report, we demonstrate that gp100-c1 cDNA encodes glycoproteins of 100 kDa (gp100) and 10 kDa (gp10) which are recognized by these mAbs in human melanoma cells. The translation product deduced from the open reading frame present in gp100-c1 cDNA is highly homologous to another melanocyte-specific protein, Pmel17. Nucleotide sequence analysis of genomic DNA indicates that the transcripts corresponding to gp100 and Pmel17 cDNAs originate from a single gene via alternative splicing. In all normal and malignant melanocytic cells analyzed, gp100 and Pmel17 RNAs are simultaneously expressed.

Amino Acid Sequence↗
PubMed1994

Mutational analysis of Agrobacterium tumefaciens pTiA6 virD1: identification of functionally important residues.

Mutagenesis experiments were used to identify functionally important regions of Agrobacterium tumefaciens pTiA6 VirD1. Random mutations were introduced by using Taq polymerase in a mutagenic reaction buffer containing manganese and altered nucleotide ratios to increase errors during the polymerase chain reaction (PCR). The mutants were assayed for VirD1-, VirD2-dependent border-nicking activity in Escherichia coli harbouring a border-containing substrate plasmid. Analysis of the mutants led to the identification of a region from amino acids 45-60 that is important for VirD1 activity. This region corresponds to a previously postulated potential DNA-binding domain. Deletion mutagenesis indicated that amino acids 2-16 could be deleted without affecting VirD1 function, whereas a larger deletion, amino acids 5-27, completely inactivated VirD1.

Agrobacterium tumefaciens↗
PubMed1993

Melanocyte lineage-specific antigens recognized by monoclonal antibodies NKI-beteb, HMB-50, and HMB-45 are encoded by a single cDNA.

The glycoproteins recognized by monoclonal antibody (MAb) NKI-beteb are among the best diagnostic markers for human melanoma. MAb NKI-beteb reacts with melanoma cells throughout tumor development and does not cross-react with other tumor or normal cells, except for cells of the melanocytic lineage. Two other melanocyte lineage-specific MAbs, HMB-50 and HMB-45, show a specificity and staining pattern strikingly similar to the ones observed for NKI-beteb. Herein, we demonstrate that all three MAbs recognize protein products encoded by a single cDNA. Expression of this cDNA in BLM cells results in immunoreactivity with all three MAbs. In addition, we demonstrate co-distribution of the RNA species detected by the cDNA with the proteins recognized by the MAbs in tissue sections.

Antibodies, Monoclonal↗
PubMed1992

Mutational analysis of Agrobacterium tumefaciens virD2: tyrosine 29 is essential for endonuclease activity.

Agrobacterium tumefaciens VirD2 polypeptide, in the presence of VirD1, catalyzes a site- and strand-specific nicking reaction at the T-DNA border sequences. VirD2 is found tightly attached to the 5' end of the nicked DNA. The protein-DNA complex is presumably formed via a tyrosine residue of VirD2 (F. Durrenberger, A. Crameri, B. Hohn, and Z. Koukolikova-Nicola, Proc. Natl. Acad. Sci. USA 86:9154-9158, 1989). A mutational approach was used to study whether a tyrosine residue(s) of VirD2 is required for its activity. By site-specific mutagenesis, a tyrosine (Y) residue at position 29, 68, 99, 119, 121, 160, or 195 of the octopine Ti plasmid pTiA6 VirD2 was altered to phenylalanine (F). The Y-29-F or Y-121-F mutation completely abolished nicking activity of VirD2 in vivo in Escherichia coli. Two other substitutions, Y-68-F and Y-160-F, drastically reduced VirD2 activity. A substitution at position 99, 119, or 195 had no effect on VirD2 activity. Additional mutagenesis experiments showed that at position 29, no other amino acid could substitute for tyrosine without destroying VirD2 activity. At position 121, only a tryptophan (W) residue could be substituted. This, however, yielded a mutant protein with significantly reduced VirD2 activity. The nicked DNA from strains bearing a Y-68-F, Y-99-F, Y-119-F, Y-160-F, Y-195-F, or Y-121-W mutation in VirD2 was always found to contain a tightly linked protein.

Agrobacterium tumefaciens↗
PubMed1992

The Agrobacterium tumefaciens virD3 gene is not essential for tumorigenicity on plants.

Genetic studies indicate that three of the four polypeptides encoded within the virD operon of the Agrobacterium tumefaciens Ti plasmid are essential for virulence. In order to determine whether the fourth polypeptide, VirD3, has any role in virulence, complementation analysis was used. An A. tumefaciens strain, A348 delta D, which lacked the entire virD operon in the Ti plasmid pTiA6, was constructed. Plasmids containing defined regions of the virD operon were introduced into this strain, and virulence was tested by the strains' abilities to form tumors on Kalanchoe leaves, tomato stems, and potato tubers. As expected, deletion of the virD operon led to an avirulent phenotype. The virulence of this strain could be restored by providing virD1, virD2, and virD4 in trans. No requirement for virD3 in tumor formation was observed in these assays.

Agrobacterium tumefaciens↗
PubMed1990

Identification of a multifunctional, cell-binding peptide sequence from the a1(NC1) of type IV collagen.

We have previously identified three distinctive amino acid sequences from type IV collagen which specifically bound to heparin and also inhibited the binding of heparin to intact type IV collagen. One of these chemically synthesized domains, peptide Hep-I, has the sequence TAGSCLRKFSTM and originates from the a1(noncollagenous [NC1]) chain of type IV collagen (Koliakos, G. G., K. K. Koliakos, L. T. Furcht, L. A. Reger, and E. C. Tsilibary. 1989. J. Biol. Chem. 264:2313-2323). We describe in this report that this same peptide also bound to intact type IV collagen in solid-phase assays, in a dose-dependent and specific manner. Interactions between peptide Hep-I and type IV collagen in solution resulted in inhibition of the assembly process of this basement membrane glycoprotein. Therefore, peptide Hep-I should represent a major recognition site in type IV collagen when this protein polymerizes to form a network. In addition, solid phase-immobilized peptide Hep-I was able to promote the adhesion and spreading of bovine aortic endothelial cells. When present in solution, peptide Hep-I competed for the binding of these cells to type IV collagen- and NC1 domain-coated substrata in a dose-dependent manner. Furthermore, radiolabeled peptide Hep-I in solution also bound to endothelial cells in a dose-dependent and specific manner. The binding of radiolabeled Hep-I to endothelial cells could be inhibited by an excess of unlabeled peptide. Finally, in the presence of heparin or chondroitin/dermatan sulfate glycosaminoglycan side chains, the binding of endothelial cells to peptide Hep-I and NC1 domain-coated substrates was also inhibited. We conclude that peptide Hep-I should have a number of functions. The role of this type IV collagen-derived sequence in such diverse phenomena as self-association, heparin binding and cell binding and adhesion makes Hep-I a crucial domain involved in the determination of basement membrane ultrastructure and cellular interactions with type IV collagen-containing matrices.

Amino Acid Sequence↗