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PubMed2002

Central obesity and risk for type 2 diabetes in Maori, Pacific, and European young men in New Zealand.

New Zealanders of Polynesian origin have a higher prevalence of obesity and type 2 diabetes mellitus than those of European origin. Risk factors for type 2 diabetes mellitus--decreased energy expenditure, increased body fat mass, and central body fat--in 30 normoglycemic Maori, Pacific, and European men were studied. Biochemical measures of risk for type 2 diabetes mellitus included an oral glucose tolerance test, insulin, lipids, and glycosylated hemoglobin. The groups did not differ significantly in BMI, height, body mass or fat mass (DEXA), or adjusted resting metabolic rate (indirect calorimetry), but the European subjects had significantly lower subscapular to triceps skinfolds and fat-free mass than the Maori and Pacific groups. Central obesity by anthropometry and DEXA showed strong associations with the biochemical measures for type 2 diabetes risk. These findings emphasize the association between body composition and central fat distribution with risk of diabetes independent of ethnicity.

Absorptiometry, Photon↗
PubMed1992

Sex and subsite frequency of large bowel cancer in the Kingdom of Saudi Arabia: a comparison with New Zealand.

New Zealand (NZ) has a high risk population for the development of large bowel cancer (LBC). The Kingdom of Saudi Arabia (KSA) has a low risk population and is estimated to have incidence and mortality rates which are ten times lower than NZ. It has already been shown that in NZ, females have a higher incidence of right-sided colonic cancer and males a higher incidence of rectal cancer. To determine whether the same situation exists in a low risk population the NZ data were compared with similar data from the cancer registry at the King Faisal Specialist Hospital and Research Center (KFSHRC). Between 1975 and 1989, 433 Saudi and Yemeni patients with LBC were registered at KPSH. The subsite distribution of tumours in this group were compared with the subsite distribution in 4678 patients registered in NZ between 1972 and 1975. The male to female (M:F) ratio for right-sided tumours in KSA was 1:0.90 compared with 1:1.56 in NZ whereas the ratios for rectal tumours were 1:0.61 and 1:0.83 respectively. This study confirms the presence of a lower frequency of right-sided tumours in females in a low risk country and further confirms the importance of gender in LBC. It may be that early and multiple child bearing, physical activity and relatively poor diets have been protective for Saudi females.

Colorectal Neoplasms↗
PubMed1984

Oral health status and tradition in New Zealand.

New Zealand in the 1930's faced a very high prevalence of caries, particularly in children, and much edentulousness in adults of all ages. There was a very large unmet treatment requirement. This led to the development of two state funded delivery systems--for children by the School Dental Service, and for adolescents by the Dental Benefit Scheme. The treatment of adults was provided in the private sector. A study in 1976 determined the standard of oral health and the treatment needs, and examined public attitudes. Comparison with previous data showed a remarkable reduction in the prevalence of caries and in the level of edentulousness. Children and adolescents had little untreated decay (D = 1.3), few extractions and large numbers of restored teeth (F = 11.9). Adults still had a high level of edentulousness. Generalized gingivitis was present in 6 per cent of the young adult group and in 20 per cent of older adults. Polynesians, the lesser educated and low socio-economic groups had more periodontal disease at all ages. Two of the goals for the year 2000 should be achieved by 1988: i.e. 50 per cent of 5-year-olds should be caries-free and 12-year-olds should have a DMFT of less than 3. Two more goals should be reached by the year 2000, i.e. 85 per cent of those aged 18 should retain all their teeth and there should be a 50 per cent reduction in edentulousness in the age group 34-44.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed2004

New loci from New Zealand Black and New Zealand White mice on chromosomes 4 and 12 contribute to lupus-like disease in the context of BALB/c.

New Zealand Black (NZB) and New Zealand White (NZW) mice are genetically predisposed to a lupus-like autoimmune syndrome. To further define the loci linked to disease traits in NZB and NZW mice in the context of the BALB/c genetic background, linkage analyses were conducted in two crosses: (NZW x BALB/c.H2(z))F(1) x NZB and (NZB x BALB/c)F(2). Novel loci linked to autoantibody production and glomerulonephritis, present in both NZB and NZW mice, were identified on proximal chromosomes 12 and 4. The chromosome 12 locus showed the strongest linkage to anti-nuclear Ab production. Additionally, a number of other novel loci linked to lupus traits derived from both the New Zealand and non-autoimmune BALB/c genomes were identified. Furthermore, we confirm the linkage of disease to a number of previously described lupus-associated loci, demonstrating that they are relatively background independent. These data provide a number of additional candidate gene regions in murine lupus, and highlight the powerful effect the non-autoimmune background strain has in influencing the genetic loci linked to disease.

Alleles↗
PubMed1990

Ly-1 B cells and disease activity in (New Zealand black x New Zealand white)F1 mice. Effect of total lymphoid irradiation.

The treatment of female (New Zealand black x New Zealand white)F1 mice with total lymphoid irradiation resulted in a prolonged remission of autoimmune disease activity. Total lymphoid irradiation-treated mice also showed a marked reduction of Ly-1 B cells, which lasted up to 3 months. The subsequent return of Ly-1 B cells to preirradiation levels was not associated with a simultaneous return of disease when measured by parameters such as IgG anti-DNA antibodies and spontaneous secretion of IgG by splenic cells. In cell sorting experiments, most of the cells spontaneously secreting IgG were found within the Ly-1- (CD5-) splenic B cell population.

Animals↗
PubMed1990

Estrogen metabolism in the (New Zealand black x New Zealand white)F1 murine model of systemic lupus erythematosus.

Hepatic microsomal estrogen metabolism was analyzed in the (New Zealand black x New Zealand white)F1 ([NZB x NZW]F1) murine model of systemic lupus erythematosus. Both the estrogen 2-hydroxylase activity (per mg microsomal protein) and the hepatic cytochrome P-450 content were higher in premorbid (NZB x NZW)F1 mice, as compared with similarly aged nonautoimmune mice. However, these differences were not associated with alterations in the relative formation of the 2-hydroxylated and the 16 alpha-hydroxylated metabolites. The development of overt nephritis was associated with a decrease in estrogen metabolic activity, but not with any alteration in the distribution of estrogen metabolites. Thus, estrogen metabolism was not altered in premorbid (NZB x NZW)F1 mice in a manner that would result in abnormal retention of hormonally active metabolites.

Animals↗
PubMed1988

Neuromuscular histopathology in (New Zealand black x New Zealand white)F1 and MRL-lpr/lpr autoimmune mice: models for skeletal muscle involvement in connective tissue disease.

Skeletal muscle from (New Zealand black x New Zealand white)F1 and MRL-lpr/lpr mice was examined for histopathologic abnormalities. Although young animals had no muscle abnormalities, older mice in both strains had the following histopathologic abnormalities: perimysial/endomysial inflammation, acute simple denervation, muscle degeneration/necrosis, and an increase in internal nuclei. MRL-lpr/lpr mice had the following additional histopathologic abnormalities: inflammatory vascular disease (vasculitis), central myofibrillar loss, fascial inflammation, and tubular aggregates. These abnormalities are comparable with those seen in human connective tissue diseases, particularly the association with inflammation. These mouse strains provide good animal models for the study of immunopathologic processes of skeletal muscle associated with connective tissue disease.

Animals↗
PubMed1998

Monoclonal anti-cardiolipin antibodies from New Zealand Black x New Zealand White F1 mice react to thrombomodulin.

The reactivity with and affinity for thrombomodulin (TM) of monoclonal anti-cardiolipin Abs (MoaCL), derived from a New Zealand Black x New Zealand White F1 (NZB/W F1) mouse, were studied to investigate the pathogenicity of anti-cardiolipin Abs (aCL). Four of eighteen MoaCL were found to react with rabbit TM when examined using ELISA. These four MoaCL also reacted with synthetic peptide that included the epidermal growth factor-like domain of human TM, a binding site for thrombin. The reaction with TM of these four MoaCL was inhibited by bovine thrombin. When the affinity for TM of the MoaCL was determined, the dissociation constants (Kd) ranged from 4.8 x 10(-9) to 4.7 x 10(-8) M. By contrast, examination of the affinity for cardiolipin (CL) gave values from 8.3 x 10(-6) to 7.4 x 10(-5) M. Thus, these MoaCL reacted to TM with a higher affinity than to CL. Moreover, these MoaCL also bound to TM on HUVEC and down-regulated the expression level of TM on the surface of HUVEC due to internalization of TM. The binding of thrombin to TM is known to initiate rapid protein C activation, and complexes of activated protein C and protein S show anticoagulatory activity. Thus, the present studies suggest that certain pathogenic aCL cross-react with TM and induce down-regulation of TM on endothelial cells, followed by induction of thrombosis.

Animals↗
PubMed2002

Control and eradication of animal diseases in New Zealand.

New Zealand is free from all the major epidemic (Office International des Epizooties List A) diseases of animals and other important diseases, such as rabies and the transmissible spongiform encephalopathies. The once endemic conditions of sheep scab (Psoroptes ovis), bovine brucellosis (Brucella abortus), hydatids (Echinococcus granulosus) and Aujeszky's disease have been eradicated. Anthrax (Bacillus anthracis) is no longer considered endemic and Pullorum disease (Salmonella Pullorum) has effectively been eradicated from commercial poultry flocks. There are current control programmes for bovine tuberculosis (Mycobacterium bovis), enzootic bovine leucosis in dairy cattle, infectious bursal disease, ovine epididymitis (Brucella ovis), and caprine arthritis encephalitis. Historically, incursions by three important non-endemic diseases, contagious bovine pleuropneumonia, classical swine fever and scrapie, have been successfully eliminated. Any new occurrence of a serious exotic disease would be dealt with swiftly using powerful legislative authorities available for the purpose.

Journal Article↗
PubMed1992

Premature death with bladder outlet obstruction and hyperprolactinemia in New Zealand black X New Zealand white mice treated with ethinyl estradiol and 17 beta-estradiol.

OBJECTIVE: To determine causes of death, estrogen toxicity, and hyperprolactinemia in a murine model of systemic lupus erythematosus (SLE). METHODS: Female New Zealand Black x New Zealand White (NZB x NZW) mice were implanted with ethinyl estradiol, 17 beta-estradiol, or empty capsules (controls). RESULTS: Estrogen-treated mice developed striking hyperprolactinemia and died prematurely with genitourinary complications. CONCLUSION: Implanted estrogens, including 17 beta-estradiol in a dose reported previously to stimulate SLE, contribute to premature death in NZB x NZW mice, through toxic effects. Estrogen therapy increases the level of prolactin, an immunostimulatory hormone.

Animals↗
PubMed1987

Monoclonal autoantibody from a (New Zealand black x New Zealand white)F1 mouse and some human scleroderma sera target an Mr 34,000 nucleolar protein of the U3 RNP particle.

A monoclonal IgG2a antinucleolar autoantibody (72B9) was obtained by fusion of spleen cells from a (New Zealand black x New Zealand white)F1 mouse with myeloma cells (P3x63Ag8.653). Antibody 72B9 recognized a highly conserved nucleolar antigen present in both animal and plant cells. The staining pattern produced by antibody 72B9 in different cell substrates was identical with those obtained by scleroderma antibodies reactive with a basic (pI 8.5) nucleolar protein of Mr 34,000, which is associated with the U3 RNP particle. Western blotting further confirmed its reactivity with this scleroderma-related U3 RNP protein.

Animals↗
PubMed2002

A novel susceptibility locus on chromosome 2 in the (New Zealand Black x New Zealand White)F1 hybrid mouse model of systemic lupus erythematosus.

Systemic lupus erythematosus (SLE) is inherited as a complex polygenic trait. (New Zealand Black (NZB) x New Zealand White (NZW)) F(1) hybrid mice develop symptoms that remarkably resemble human SLE, but (NZB x PL/J)F(1) hybrids do not develop lupus. Our study was conducted using (NZW x PL/J)F(1) x NZB (BWP) mice to determine the effects of the PL/J and the NZW genome on disease. Forty-five percent of BWP female mice had significant proteinuria and 25% died before 12 mo of age compared with (NZB x NZW)F(1) mice in which >90% developed severe renal disease and died before 12 mo. The analysis of BWP mice revealed a novel locus (chi(2) = 25.0; p < 1 x 10(-6); log of likelihood = 6.6 for mortality) designated Wbw1 on chromosome 2, which apparently plays an important role in the development of the disease. We also observed that both H-2 class II (the u haplotype) and TNF-alpha (TNF(z) allele) appear to contribute to the disease. A suggestive linkage to proteinuria and death was found for an NZW allele (designated Wbw2) telomeric to the H-2 locus. The NZW allele that overlaps with the previously described locus Sle1c at the telomeric part of chromosome 1 was associated with antinuclear autoantibody production in the present study. Furthermore, the previously identified Sle and Lbw susceptibility loci were associated with an increased incidence of disease. Thus, multiple NZW alleles including the Wbw1 allele discovered in this study contribute to disease induction, in conjunction with the NZB genome, and the PL/J genome appears to be protective.

Alleles↗
PubMed2004

Toxoplasma gondii infection inhibits the development of lupus-like syndrome in autoimmune (New Zealand Black x New Zealand White) F1 mice.

Systemic lupus erythematosus (SLE) is an autoimmune disease characterized by the presence of autoantibodies and lupus nephritis. In the present study using New Zealand Black (NZB) x New Zealand White (NZW) F1 (NZBW F1) mice, we planned to investigate the effects of Toxoplasma gondii infection on the progress of lupus nephritis. Female NZBW F1 mice at the age of 2 months were perorally infected with T. gondii. The T. gondii infection reduced the number of mice developing proteinuria and immune complex deposits in their kidneys and prolonged their life span. A marked decrease in the levels of IgM and IgG anti-DNA antibodies, especially IgG2a and IgG3 subclasses, was observed in T. gondii-infected NZBW F1 mice at 9 months of age. The level of anti-HSP70 IgG autoantibody in the sera of NZBW F1 mice was significantly higher than that in control mice at 9 weeks after T. gondii infection. Moreover, NZBW F1 mice treated with anti-self heat shock protein 70 (HSP70) monoclonal antibody were substantially protected against the onset of glomerulonephritis. Further, down-regulation of intracellular expression of IFN-gamma and IL-10 was shown in spleen cells of T. gondii-infected NZBW F1 mice. This was consistent with the previous data indicating the involvement of Th1-type and Th2-type cytokines in the development of lupus-like nephritis. These results suggest that T. gondii infection is capable of preventing the development of autoimmune renal disorder in NZBW F1 mice.

Animals↗
PubMed1996

Anti-CD40 ligand antibody treatment prevents the development of lupus-like nephritis in a subset of New Zealand black x New Zealand white mice. Response correlates with the absence of an anti-antibody response.

Systemic lupus erythematosus is characterized by B cell production of pathogenic autoantibodies dependent upon cooperation from CD4+ Th cells. The interaction between CD40 on B cells and CD40 ligand (CD40L) on Th cells is necessary for normal thymus-dependent Ab production. An anti-murine CD40L mAb blocks binding of CD40L to CD40 and prevents primary and secondary immune responses to thymus-dependent Ags. In this study, New Zealand Black x New Zealand White lupus-prone mice treated with this anti-CD40L Ab from ages 4 to 10 mo had reduced anti-DNA autoantibody production and renal disease and significantly prolonged survival compared with control mice. Pathologic examination verified the absence of significant renal damage or immune deposition in responding mice. Mice that responded to treatment did not develop an Ab response to the administered Ab. Long-term survivors mounted a substantial Ab response to keyhole limpet hemocyanin after completion of anti-CD40L Ab treatment, suggesting that some of the immunosuppressive effects of the Ab may be reversible. These results suggest a human form of this Ab may have therapeutic utility in human systemic lupus erythematosus.

Animals↗
PubMed2004

Ig-reactive CD4+CD25+ T cells from tolerized (New Zealand Black x New Zealand White)F1 mice suppress in vitro production of antibodies to DNA.

We have recently shown that tolerogenic administration of an artificial peptide (pConsensus) that is based on sequences within the V(H) regions of several murine anti-dsDNA Ig delays appearance of autoantibodies in female (New Zealand Black (NZB) x New Zealand White (NZW))F(1) (NZB/W F(1)) mice and significantly prolongs their survival. The aim of this study was to characterize the T cell population(s) involved in pConsensus-induced down-regulation of autoimmune responses in tolerized NZB/W F(1) mice. Using MHC class II dimers loaded with tolerogenic peptide, we found that pCons favored expansion of peptide-reactive CD4(+)CD25(+) regulatory T cells (T(R)) that inhibited in vitro production of anti-dsDNA Ab-forming cells. Suppression by T(R) was abrogated by the presence in culture of Ab to glucocorticoid-induced TNFR family member 18 or to TGFbeta latency-associated protein. These findings suggest possible relevance of Ag specificity in the mechanism of T(R)-mediated immune tolerance to Ig-derived peptides in NZB/W F(1) mice.

Animals↗
PubMed2005

IFN-alpha induces early lethal lupus in preautoimmune (New Zealand Black x New Zealand White) F1 but not in BALB/c mice.

Recent studies indicate that IFN-alpha is involved in pathogenesis of systemic lupus erythematosus. However, direct proof that IFN-alpha is not only necessary, but also sufficient to induce lupus pathogenicity is lacking. In this study, we show that in vivo adenovector-mediated delivery of murine IFN-alpha results in preautoimmune (New Zealand Black (NZB) x New Zealand White (NZW))F(1), but not in normal, mice, in a rapid and severe disease with all characteristics of systemic lupus erythematosus. Anti-dsDNA Abs appeared as soon as day 10 after initiation of IFN-alpha treatment. Proteinuria and death caused by glomerulonephritis occurred in all treated mice within, respectively, approximately 9 and approximately 18 wk, at a time when all untreated (NZB x NZW)F(1) did not show any sign of disease. IFN-alpha in vivo induced an overexpression of B lymphocyte stimulator in circulation at similar levels in both the preautoimmune and the normal mouse strains. All effects elicited by IFN-alpha were dose dependent. (NZB x NZW)F(1) infused with purified murine IFN-alpha also showed acceleration of lupus. Thus, prolonged expression of IFN-alpha in vivo induces early lethal lupus in susceptible animals.

Animals↗
PubMed2003

CD4+ T cells from (New Zealand Black x New Zealand White)F1 lupus mice and normal mice immunized against apoptotic nucleosomes recognize similar Th cell epitopes in the C terminus of histone H3.

We have previously reported that peptide 88-99 of histone H4 represents a minimal T cell epitope recognized by Th cells from nonautoimmune BALB/c (H-2(d/d)) mice immunized with nucleosomes. In this study, we tested a panel of overlapping peptides spanning the whole sequences of H4 and H3 for recognition by CD4(+) T cells from unprimed (New Zealand Black (NZB) x New Zealand White (NZW))F(1) lupus mice (H-2(d/z)). None of the 11 H4 peptides was recognized by CD4(+) T cells from (NZB x NZW)F(1) mice. In contrast, these cells proliferated and secreted IL-2, IL-10, and IFN-gamma upon ex vivo stimulation with H3 peptides representing sequences 53-70, 64-78, and 68-85. Peptides 56-73 and 61-78 induced the production of IFN-gamma and IL-10, respectively, without detectable proliferation, suggesting that they may act as partial agonist of the TCR. Th cells from unprimed BALB/c mice and other lupus-prone mice such as SNF(1) (H-2(d/q)) and MRL/lpr (H-2(k/k)) mice did not recognize any peptides present within the H3 region 53-85. We further demonstrated that immunization of normal BALB/c mice with syngeneic liver nucleosomes and spleen apoptotic cells, but not with nonapoptotic syngeneic cells, induced Th cell responses against several peptides of the H3 region 53-85. Moreover, we found that this conserved region of H3, which is accessible at the surface of nucleosomes, is targeted by Abs from (NZB x NZW)F(1) mice and lupus patients, and contains motifs recognized by several distinct HLA-DR molecules. It might thus be important in the self-tolerance breakdown in lupus.

Amino Acid Sequence↗
PubMed2005

Expansion and hyperactivity of CD1d-restricted NKT cells during the progression of systemic lupus erythematosus in (New Zealand Black x New Zealand White)F1 mice.

CD1d-restricted NKT cells expressing invariant TCR alpha-chain rearrangements (iNKT cells) have been reported to be deficient in humans with a variety of autoimmune syndromes and in certain strains of autoimmune mice. In addition, injection of mice with alpha-galactosylceramide, a specific glycolipid agonist of iNKT cells, activates these T cells and ameliorates autoimmunity in several different disease models. Thus, deficiency and reduced function in iNKT cells are considered to be risk factors for the development of such diseases. In this study we report that the development of systemic lupus erythematosus in (New Zealand Black (NZB) x New Zealand White (NZW))F(1) mice was paradoxically associated with an expansion and activation of iNKT cells. Although young (NZB x NZW)F(1) mice had normal levels of iNKT cells, these expanded with age and became phenotypically and functionally hyperactive. Activation of iNKT cells in (NZB x NZW)F(1) mice in vivo or in vitro with alpha-galactosylceramide indicated that the immunoregulatory role of iNKT cells varied over time, revealing a marked increase in their potential to contribute to production of IFN-gamma with advancing age and disease progression. This evolution of iNKT cell function during the progression of autoimmunity may have important implications for the mechanism of disease in this model of systemic lupus erythematosus and for the development of therapies using iNKT cell agonists.

Animals↗