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Biomedical subjects

A Cox

Publications and source records attributed to A Cox.

At least 73 records · Page 4Linked to original sources
PubMed1999

Combined sib-TDT and TDT provide evidence for linkage of the interleukin-1 gene cluster to erosive rheumatoid arthritis.

Rheumatoid arthritis (RA) is a common disease of unknown aetiology which usually causes progressive destruction of the joints. Familial aggregation, twin studies and segregation analyses suggest that there is a genetic component to RA and the HLA-DRB1 locus in the major histocompatibility complex on chromosome 6 has been shown to be linked to, and associated with, RA susceptibility. It is likely that other genes with weaker effects are also involved, which may be difficult to detect using conventional parametric and non-parametric linkage methods. We have implemented the combined sib-TDT and TDT, in addition to parametric and non-parametric linkage methods, to investigate the candidate genes of the interleukin-1 (IL-1) gene cluster on chromosome region 2q13, since IL-1 is an important cytokine in the control of the inflammatory response that is central to RA pathology. Several tightly linked IL-1 cluster markers yielded suggestive evidence for linkage in the combined TDT in those families in which affected siblings did not share two HLA-DRB1 alleles identical by descent. The evidence was significant in those with severe disease, as assessed by the presence of bone erosions. In contrast, there was no evidence of linkage using non-parametric linkage analysis, but parametric analysis revealed weak evidence of linkage when marker-trait disequilibrium was incorporated into the analysis. The data provide preliminary evidence for linkage of genes of the IL-1 cluster to RA and suggest a possible role for this region in severe erosive disease.

Arthritis, Rheumatoid↗
PubMed1999

Autism spectrum disorders at 20 and 42 months of age: stability of clinical and ADI-R diagnosis.

The association between, and stability of, clinical diagnosis and diagnosis derived from the Autism Diagnostic Interview-Revised (ADI-R; Lord, Rutter, & Le Couteur, 1994) was examined in a sample of prospectively identified children with childhood autism and other pervasive developmental disorders assessed at the age of 20 months and 42 months. Clinical diagnosis of autism was stable, with all children diagnosed with childhood autism at age 20 months receiving a diagnosis of childhood autism or a related pervasive developmental disorder (PDD) at age 42 months. Clinical diagnosis of childhood autism was also reasonably sensitive, with all children who went on to receive a clinical diagnosis of childhood autism at 42 months being identified as having autism or PDD at 20 months. However, clinical diagnosis for PDD and Asperger's syndrome lacked sensitivity at 20 months, with several children who subsequently received these diagnoses at 42 months receiving diagnoses of language disorder or general developmental delay, as well as in two cases being considered clinically normal, at the earlier timepoint. The ADI-R was found to have good specificity but poor sensitivity at detecting childhood autism at 20 months; however, the stability of diagnosis from 20 to 42 months was good. In addition, the ADI-R at age 20 months was not sensitive to the detection of related PDDs or Asperger's syndrome. The continuity and discontinuity between behavioural abnormalities identified at both timepoints in the three domains of impairment in autism was examined, both in children who met final clinical criteria for an autistic spectrum disorder, and for children with language disorder who did not, as well as for a small sample of typically developing children.

Autistic Disorder↗
PubMed1998

The distribution of lead within ancient and modern human teeth: implications for long-term and historical exposure monitoring.

The preservation of lead within human tissue makes it possible to monitor long-term exposure to the element and to model changing sources of lead pollution throughout the lifetime of an individual. Dental tissues have recently been shown to be particularly useful for this purpose. Enamel, for instance, forms at known stages of life and is chemically stable in vivo whereas dentine is remodelled in a predictable fashion. The relative stability of enamel is reflected in its excellent post-mortem preservation. This raises the possibility of using historical or archaeological material to reconstruct long-term trends and establish baseline data relating to exposure among pre-industrial or even prehistoric populations. The use of archaeological material is currently problematic, however, because of the site-specific nature of diagenesis and incomplete understanding of its chemistry, particularly in respect of lead uptake into dental tissue from the burial environment. A detailed study of lead distribution within both ancient and modern human teeth is presented. Conclusions are drawn on the pattern of lead distribution resulting from tissue formation and the manner of its alteration in the burial environment. In particular, attention is drawn to a consistent enrichment of lead within the outer 30 microns of the enamel of both ancient and modern teeth which appears to be unrelated to diagenesis. The implications for current approaches to long-term monitoring and for the reconstruction of historical and archaeological exposure patterns are discussed.

Archaeology↗
PubMed1998

Inhibition of cromolyn-induced phosphorylation of a 78-kDa protein by phorbol esters in rat peritoneal mast cells.

Disodium cromoglycate (cromolyn) is a well documented inhibitor of immunologically-induced histamine release from rat peritoneal mast cells and has been shown to stimulate the phosphorylation of a mast cell protein of apparent molecular mass 78,000 Da (78 kDa), an event which may be involved in terminating secretion. Here we aimed to determine the role of the ubiquitous enzyme, protein kinase C, in the phosphorylating activity of cromolyn by examining the effects of phorbol esters (activators of protein kinase C) on protein phosphorylation in [32P]orthophosphate loaded rat peritoneal mast cells. Protein kinase C-activating phorbol esters such as 12-O-tetradecanoyl phorbol-13-acetate (TPA) and 4beta-phorbol 12,13-dibutyrate (PdBu) were found to potently inhibit cromolyn-induced phosphorylation when added to mast cells simultaneously with cromolyn (IC50 22 and 79 nM respectively). 4Alpha-phorbol 12,13-didecanoate (PdD), a phorbol ester which does not activate protein kinase C, had no effect on cromolyn-induced phosphorylation. Addition of TPA to mast cells previously exposed to cromolyn for 60 sec (i.e. when 78-kDa protein phosphorylation is maximal) also caused a very rapid dephosphorylation of the 78-kDa protein. Phosphorylation of the 78-kDa protein can also be induced by dibutyryl cyclic GMP and this action was similarly inhibited by TPA and PdBu. Cromolyn inhibited secretion induced by anti-IgE, but not by TPA, and thus inhibition of secretion by cromolyn is further correlated to its phosphorylation of the 78-kDa protein. The data suggest that the inhibitory action of cromolyn on mast cell secretion and phosphorylation of the 78-kDa protein are not mediated through a phorbol ester-sensitive protein kinase C, but more likely that such an enzyme could be involved in regulating dephosphorylation of the 78-kDa protein. Further explanations for this novel dephosphorylating activity of phorbol esters are discussed.

Animals↗
PubMed1998

Psychological disturbance and child sexual abuse: a follow-up study.

OBJECTIVE: The aim of this prospective study was to identify risk factors for the development of psychological disturbance in sexually abused children, enabling recognition of the need for appropriate psychological intervention and provision. METHOD: A city-wide study of children aged 16 or under was carried out, with all cases of CSA requiring investigation within 12 months included. Data were collected on 144 children from police, social services, and pediatricians. Follow-up was by questionnaire and interview with involved professionals at 4 weeks, 9 months, and 2 years post investigation. RESULTS: Initially, two-thirds of children showed emotional or behavioral indicators of disturbance, commonly sleep disturbance, temper tantrums, and depression. Over time, there was a substantial increase, with anxiety and depression, suicide attempts, substance abuse, lack of interaction with peers and sexualized behavior showing increases over the study's duration. Age, gender, abuse, and perpetrator characteristics did not show strong effects initially. Children involved in criminal proceedings were at particular risk. No improvement was evident over time. CONCLUSIONS: In the absence of clear risk factors other than initial disturbance, process models involving cognitive factors may be helpful in explaining disturbance, and the need for early identification of disturbance and intervention is highlighted.

Adolescent↗
PubMed1998

Renal expression of transforming growth factor-beta inducible gene-h3 (beta ig-h3) in normal and diabetic rats.

BACKGROUND: Transforming growth factor-beta (TGF-beta) has been implicated in the pathogenesis of a number of kidney diseases characterized by glomerulosclerosis and tubulointerstitial fibrosis. TGF-beta is secreted in a latent form requiring extracellular modification to become biologically active. TGF-beta inducible gene-h3 (beta ig-h3) is a recently identified TGF-beta-induced gene product. The present study sought to examine beta ig-h3 expression in normal and diabetic rats. METHODS: Beta ig-h3, TGF-beta1 and alpha1 (IV) collagen gene expression were assessed by Northern blot analysis and in situ hybridization in 20 Sprague Dawley rats, randomly assigned to receive streptozotocin (diabetic, N = 11) or citrate buffer alone (control, N = 9) and sacrificed eight months later. The effect of exogenous TGF-beta1 on beta ig-h3 expression was also assessed in cultured proximal tubular cells. RESULTS: In situ hybridization localized beta ig-h3 gene expression to the juxtaglomerular apparatus and the pars recta (S3 segment) of proximal tubules in both control and diabetic animals. Kidney TGF-beta 1, beta ig-h3 and alpha1 (IV) collagen mRNA from diabetic rats were increased two- to threefold compared with controls (P < 0.01). There was a significant correlation between TGF-beta1 and beta ig-h3 gene expression in kidneys from diabetic rats (r = 0.73, P = 0.01). In addition, beta ig-h3 mRNA increased in response to exogenous TGF-beta1 in a dose-dependent fashion in cultured proximal tubular cells. CONCLUSION: These findings support the hypothesis that biologically active TGF-beta plays a pathogenetic role in diabetic kidney disease and suggest that beta ig-h3 may be a useful index of TGF-beta1 bioactivity in the kidney.

Animals↗
PubMed1998

An analysis of linkage disequilibrium in the interleukin-1 gene cluster, using a novel grouping method for multiallelic markers.

In population- and family-based association studies, it is useful to have some knowledge of the patterns of linkage disequilibrium that exist between markers in candidate regions. When such studies are carried out with multiallelic markers, it is often convenient to group the alleles into a biallelic system, for analysis. In this study, we specifically examined the interleukin-1 (IL-1) gene cluster on chromosome 2, a region containing candidates for many inflammatory and autoimmune disorders. Data were collected on eight markers, four of which were multiallelic. Using these data, we investigated the effect of three allele-grouping strategies, including a novel method, on the detection of linkage disequilibrium. The novel approach, termed the "delta method," measures the deviation from the expected haplotype frequencies under linkage equilibrium, for each allelic combination. This information is then used to group the alleles, in an attempt to avoid the grouping together of alleles at one locus that are in opposite disequilibrium with the same allele at the second locus. The estimate haplotype frequencies (EH) program was used to estimate haplotype frequencies and the disequilibrium measure. In our data it was found that the delta method compared well with the other two strategies. Using this method, we found that there was a reasonable correlation between disequilibrium and physical distance in the region (r=-.540, P=.001, one-tailed). We also identified a common, eight-locus haplotype of the IL-1 gene cluster.

Alleles↗
PubMed1998

Angiotensin converting enzyme inhibition reduces the expression of transforming growth factor-beta1 and type IV collagen in diabetic vasculopathy.

OBJECTIVE: The purpose of this study was to assess the role of transforming growth factor (TGF)-beta1 in the development of diabetes-associated mesenteric vascular hypertrophy and in the antitrophic effect of angiotensin converting enzyme inhibitors. DESIGN AND METHODS: Streptozotocin-induced diabetic and control Sprague-Dawley rats were randomly allocated to treatment with the angiotensin converting enzyme inhibitor ramipril or to no treatment and were killed 1 or 3 weeks after the streptozotocin injection. Blood was collected and mesenteric vessels removed. Mesenteric vascular weight was measured and TGF-beta1 and alpha1 (type IV) collagen messenger (m)RNA levels were analysed by Northern analysis. Immunohistochemical analyses for TGF-beta1 and type IV collagen were also performed. RESULTS: The diabetic rats had increased mesenteric vessel weight at 3 weeks but not at 1 week and a concomitant rise in mesenteric TGF-beta1 and in alpha1 (type IV) collagen mRNA levels. Ramipril treatment attenuated mesenteric vessel hypertrophy and prevented the increase in TGF-beta1 and alpha1 (type IV) collagen mRNA levels after 3 weeks of diabetes. The immunohistochemical analysis revealed that diabetes was associated with increased TGF-beta1 and type IV collagen protein and extracellular matrix accumulation in mesenteric vessels, and this increase was reduced by ramipril treatment. CONCLUSIONS: These results support the concept that TGF-beta is involved in the changes associated with diabetic vascular disease, and suggest a mechanism by which angiotensin converting enzyme inhibitors exert their antitrophic effects.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed1998

Enhanced myelotoxicity due to granulocyte colony-stimulating factor administration until 48 hours before the next chemotherapy course in patients with small-cell lung carcinoma.

PURPOSE: To evaluate the impact of granulocyte colony-stimulating factor (G-CSF) priming on peripheral-blood cell counts during standard-dose chemotherapy. PATIENTS AND METHODS: Twelve patients with relapsed small-cell lung carcinoma (SCLC) were treated with two chemotherapy courses. Six patients received G-CSF priming only before the first course (group A) and the other six patients only before the second course (group B). Each patient served as his own control. Patients were treated with cyclophosphamide, epirubicin, and etoposide (CEE), or with vincristine, ifosfamide, mesna, and carboplatin (VIMP) every 4 weeks. G-CSF was administered subcutaneously 5 microg/kg/d for 6 days until 48 hours before the first or second chemotherapy course. RESULTS: Priming caused a lowering of the WBC nadir, with a median value of 0.95 x 10(9)/L (P = .004), and of absolute neutrophil nadir, with a median value of 0.48 x 10(9)/L (P = .03). There was a trend for a lower platelet (PLT) nadir after G-CSF priming (P = .09). G-CSF priming resulted in a prolonged duration of WBC count less than 3.0 x 10(9)/L of +4.25 days (P = .04), and of WBC count less than 1.0 x 10(9)/L of +0.50 days (P = .03). The duration of neutropenia less than 0.5 x 10(9)/L seemed longer in primed courses (+3.75 days, P = .18). The duration of PLT counts less than 100 x 10(9)/L was prolonged by 1.5 days (P = .04). Hemoglobin (Hgb) levels were not influenced by G-CSF priming. CONCLUSION: G-CSF administration until 48 hours before the next chemotherapy course increases chemotherapy-associated leukocytopenia and thrombocytopenia. This may be of special concern when G-CSF is administered during dose-densified chemotherapy.

Antineoplastic Combined Chemotherapy Protocols↗
PubMed1998

Expression of transforming growth factor-beta1 and type IV collagen in the renal tubulointerstitium in experimental diabetes: effects of ACE inhibition.

Transforming growth factor-beta (TGF-beta) and the renin-angiotensin system (RAS) have both been implicated in the pathogenesis of glomerulosclerosis in diabetic kidney disease. However, tubulointerstitial pathology may also be an important determinant of progressive renal dysfunction in diabetic nephropathy. In the present study, we investigated tubulointerstitial injury, TGF-beta1 expression, and the effect of blocking the RAS by inhibition of ACE. We randomized 36 male SD rats to control and diabetic groups. Diabetes was induced in 24 rats by administration of streptozotocin; 12 diabetic rats were further randomized to receive the ACE inhibitor ramipril (3 mg/l drinking water). At 6 months, experimental diabetes was associated with tubulointerstitial damage, a 70% increase in expression of TGF-beta1 (P < 0.05 vs. control), and a 120% increase in alpha1 (IV) collagen gene expression (P < 0.01 vs. control). In situ hybridization demonstrated a diffuse increase in both TGF-beta1 and alpha1 (IV) collagen mRNA in renal tubules. In addition, intense expression of both transcripts was noted in regions of focal tubular dilatation. Administration of the ACE inhibitor ramipril prevented tubulointerstitial injury and the overexpression of TGF-beta1 and alpha1 (IV) collagen mRNA. Changes in gene expression were accompanied by parallel changes in immunostaining for TGF-beta1 and type IV collagen. The observed beneficial effects of ramipril on the tubulointerstitium in experimental diabetes suggest that this mechanism may contribute to the therapeutic effect of ACE inhibitors in diabetic nephropathy.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed1998

The frequency and distribution of spontaneous attention shifts between social and nonsocial stimuli in autistic, typically developing, and nonautistic developmentally delayed infants.

Spontaneous shifts of attention were observed in autistic, typically developing, and nonautistic developmentally delayed infants. Three types of attention shifting behaviour were observed; (1) between an object and another object, (2) between an object and a person, and (3) between a person and another person. The two control groups shifted attention more frequently between an object and a person than between an object and another object or between a person and another person. The infants with autism showed a different pattern, shifting attention between an object and another object more than any other type of shift. Furthermore, infants with autism showed fewer shifts of attention between an object and a person, and between person and person, than did the two control groups. They also spent less time overall looking at people and looked more briefly at people and for longer durations at objects, compared to the two control groups. These results indicate an abnormality in social orientation in autism even at the early age of 20 months.

Attention↗
PubMed1998

An increase in endothelial intracellular calcium and F-actin precedes the extravasation of interleukin-2-activated lymphocytes.

OBJECTIVE: Interleukin-2 (IL-2) induces protein leakage from the microcirculation and activates lymphocytes; yet it is unclear how it alters endothelial barrier function. Here, we report of a new continuous monitoring system that allows for the continuous measurement and correlation of endothelial calcium, permeability to albumin, and extravasation of lymphocytes. METHODS: IL-2 activated lymphocytes (IL-2 LYMPH) or unstimulated lymphocytes (LYMPH) were co-incubated with human microvascular endothelial cells (HMVEC). Endothelial albumin permeability, lymphocyte extravasation intracellular calcium mobilization, and f-actin distribution were examined using a new continuous monitoring system. RESULTS: The clearance rate of fluorescein isothiocyanate-labeled-human serum albumin (FITC-HSA) in the presence of IL-2 LYMPH peaked at 20 minutes, whereas the clearance rate of LYMPH peaked at 40 minutes. Approximately 40 minutes after the peak in the clearance rate to albumin, extravasation of carboxyfluorescein-labeled lymphocytes was detected. Peak clearance rates for the extravasation of IL-2 LYMPH occurred at approximately 40 minutes after the addition of the lymphocytes to the HMVEC, whereas the peak clearance rate for the LYMPH occurred at 60 minutes after their addition. Both FITC-HSA and lymphocyte extravasation were measured concurrent to endothelial intracellular calcium mobilization by FURA-2. There was an increase in calcium activation after the addition of IL-2 stimulated lymphocytes (71 +/- 5.1 nmol/L to 185 +/- 18.9 nmol/L) compared with unstimulated lymphocytes (71 +/- 5.1 nmol/L to 110 +/- 12.2 nmol/L). The addition of IL-2 had little or no effect on endothelial actin, whereas the unstimulated lymphocytes and, to a greater extent, IL-2 LYMPH increased the presence of transversing stress fibers and decreased peripheral actin. CONCLUSIONS: The findings reported here suggest that the permeability and extravasation events that occur upon addition of lymphocytes proceeds by a calcium- and actin-dependent mechanism and that incubation of lymphocytes with IL-2 enhances normal lymphocyte mechanisms of extravasation.

Actins↗
PubMed1998

Vascular endothelial growth factor and its receptors in control and diabetic rat eyes.

Vascular endothelial growth factor (VEGF) is an endothelial cell-specific angiogenic and permeability-inducing factor that has been implicated in the pathogenesis of diabetic retinopathy. In the present study, the localization and magnitude of VEGF, VEGF receptor-1 (VEGFR-1), and VEGF receptor-2 (VEGFR-2) gene expression were examined in the eye of streptozotocin-induced diabetic rats using quantitative in situ hybridization. VEGF protein was also examined by immunohistochemistry. Abundant VEGF mRNA and protein were present in the retinae of control rats. In the retinae of diabetic rats, VEGF gene expression was increased compared with control animals (p = 0.001). The increase in VEGF mRNA was noted in the ganglion cell layer and inner nuclear layer but not in the pigment epithelium of the retina. VEGF was also detected in blood vessels, ciliary body, and lens epithelium in both control and diabetic rats. The distributions of VEGFR-1 and VEGFR-2 were similar in both control and diabetic rats. VEGFR-1 mRNA was present beneath the inner limiting membrane and in the ganglion cell layer, inner nuclear layer, outer plexiform layer, and outer limiting membrane of the retina; it was also detected in blood vessels, the ciliary body, and the cornea. The magnitude and distribution of ocular VEGFR-1 mRNA were not affected by experimental diabetes. Expression of VEGFR-2 mRNA was noted in the inner nuclear layer and pigment epithelium of the retina and in blood vessels. An increase in VEGFR-2 mRNA in the diabetic retina was restricted to the inner nuclear layer. The presence of VEGF and its receptors in the control retina suggests a physiologic role for VEGF within the eye. The changes in retinal expression of VEGF and VEGFR-2 in association with diabetes suggest a role for this pathway in diabetic retinopathy.

Animals↗
PubMed1998

[Molecular phylogeny of the nuclear 5.8S ribosomal RNA genes in 37 species of Nicotiana genus].

The primary structure of the 5.8S rRNA gene was established in 37 species of the genus Nicotiana representing four different sections of the subgenus Petuniodes: Acuminatae, Alatae, Noctiflorae, and Suaveolentes. On the basis of these data, phylogenetic analysis was performed. The obtained results are in good agreement with the modern systematics of the genus. However, the bootstrap analysis gives only poor statistical support for the branches of the phylogenetic tree owing to a small number of phylogenetically informative positions.

Base Sequence↗
PubMed1997

The role of transglutaminase in the rat subtotal nephrectomy model of renal fibrosis.

Tissue transglutaminase is a calcium-dependent enzyme that catalyzes the cross-linking of polypeptide chains, including those of extracellular matrix (ECM) proteins, through the formation of epsilon-(gamma-glutamyl) lysine bonds. This crosslinking leads to the formation of protein polymers that are highly resistant to degradation. As a consequence, the enzyme has been implicated in the deposition of ECM protein in fibrotic diseases such as pulmonary fibrosis and atherosclerosis. In this study, we have investigated the involvement of tissue transglutaminase in the development of kidney fibrosis in adult male Wistar rats submitted to subtotal nephrectomy (SNx). Groups of six rats were killed on days 7, 30, 90, and 120 after SNx. As previously described, these rats developed progressive glomerulosclerosis and tubulo-interstitial fibrosis. The tissue level of epsilon-(gamma-glutamyl) lysine cross-link (as determined by exhaustive proteolytic digestion followed by cation exchange chromatography) increased from 3.47+/- 0.94 (mean+/-SEM) in controls to 13.24+/-1.43 nmol/g protein 90 d after SNx, P </= 0.01. Levels of epsilon-(gamma-glutamyl) lysine cross-link correlated well with the renal fibrosis score throughout the 120 observation days (r = 0.78, P </= 0.01). Tissue homogenates showed no significant change in overall transglutaminase activity (14C putrescine incorporation assay) unless adjusted for the loss of viable tubule cells, when an increase from 5.77+/-0.35 to 13.93+/-4.21 U/mg DNA in cytosolic tissue transglutaminase activity was seen. This increase was supported by Western blot analysis, showing a parallel increase in renal tissue transglutaminase content. Immunohistochemistry demonstrated that this large increase in epsilon-(gamma-glutamyl) lysine cross-link and tissue transglutaminase took place predominantly in the cytoplasm of tubular cells, while immunofluorescence also showed low levels of the epsilon-(gamma-glutamyl) lysine cross-link in the extracellular renal interstitial space. The number of cells showing increases in tissue transglutaminase and its cross-link product, epsilon-(gamma-glutamyl) lysine appeared greater than those showing signs of typical apoptosis as determined by in situ end-labeling. This observed association between tissue transglutaminase, epsilon-(gamma-glutamyl) lysine cross-link, and renal tubulointerstitial scarring in rats submitted to SNx suggests that tissue transglutaminase may play an important role in the development of experimental renal fibrosis and the associated loss of tubule integrity.

Animals↗
PubMed1997

Molecular cloning of the interleukin-1 gene cluster: construction of an integrated YAC/PAC contig and a partial transcriptional map in the region of chromosome 2q13.

Genes of the interleukin-1 (IL-1) gene cluster localized on chromosome 2q13 are implicated in many physiological and pathophysiological processes. We present here a high-resolution physical map of this region between markers D2S2008 and D2S4/PAX8. An integrated YAC/PAC contig and a partial transcriptional map were constructed by STS-constent mapping using the CEPH YAC library and three PAC libraries. A total of 3 YACs, 34 PACs, and 56 STSs were integrated: 33 newly generated probes to PAC end sequences, 9 polymorphic and 4 nonpolymorphic markers, 5 known genes, 4 expressed sequence tags, and 1 pseudogene. Within the map, a complete PAC contig of > 1 Mb encompasses the IL-1 gene cluster and PAX8, a paired-box-containing gene. This allowed us to define the transcriptional orientation of GLVR1, IL1B, and IL1RN and to show that PAX8 is localized outside the IL-1 gene cluster. FISH analysis localized PAC clones containing the IL-1 gene cluster to 2q12-q13. The data provide the basis for further characterization of the IL-1 gene cluster and for the construction of a sequence-ready PAC contig of this region.

Base Sequence↗
PubMed1997

Home birth in New Zealand 1973-93: incidence and mortality.

AIMS: To determine for the period 1973-93, national and regional (1991 and 1992 only) incidence of home birth in New Zealand, with home birth defined as home being the intended place of birth at the onset of labour, to calculate perinatal and maternal mortality rates for home birth, and to categorise the cause of perinatal death. METHODS: Data sheets for 9776 planned home births were analysed. These had been collected by the Home Birth Associations of New Zealand/Aotearoa. National perinatal data and data from National Women's Hospital, Auckland were used for comparison. Trend analysis was performed by Poisson regression allowing for overdispersion. RESULTS: Planned home birth made up 2% of the total births in 1993, up from 0.04% in 1973. The home birth perinatal mortality rate for this period was 2.97 per 1000 total births, with no change over time. This was not significantly different from the rate for a selected low risk group at National Women's Hospital. Lethal anomalies caused 31% of the perinatal deaths. There was one maternal death (maternal mortality rate: 1.02 per 10,000 total births). There were significant differences in the rate of home birth in separate area health board regions for 1991 and 1992. CONCLUSION: Home birth was a safe and increasingly popular: though minor, option for New Zealand women from 1973-93.

Cause of Death↗