Beck, DA, Brady, BHG & Grant, DR 1997, 'Induced stress and microseismicity in the 3000 Orebody, Mount Isa', Geotechnical and Geological Engineering, vol. 15, no. 3, pp. 221-233.
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The 3000 Orebody is one of two orebodies in the Deep Copper Mine at Mount Isa, Australia. Owing to concerns about potential shaft pillar instabilities, an integrated seismic system was introduced to monitor seismic activity associated with pillar and country rock deformation. Coupled with numerical modelling of the stress regime, the system may assist in the characterization of rock mass damage resulting from mining, and perhaps the identification of near- and far-field geological structures that affect slope performance. A study was undertaken to quantify the seismicity and to determine potential applications of the seismic technology. The relation between geological structure and seismicity is strong, suggesting good prospects for the use of the system in the ground-control activities noted above. The induction of seismicity, which involves small magnitude events, is associated with reduction of normal stress on planes of weakness, suggesting that stress path may be an important factor in the level of seismicity observed in hard rock mines.
Howard, GM, Nguyen, TV, Pocock, NA, Kelly, PJ & Eisman, JA 1997, 'Influence of handedness on calcaneal ultrasound: Implications for assessment of osteoporosis and study design', Osteoporosis International, vol. 7, no. 3, pp. 190-194.
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Hutvágner, G, Barta, E & Bánfalvi, Z 1997, 'Isolation and sequence analysis of a cDNA and a related gene for cytochrome P450 proteins from Solanum chacoense', Gene, vol. 188, no. 2, pp. 247-252.
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Inosine-containing degenerate PCR primers corresponding to the heme-binding domain of cytochrome P450 proteins have been synthesized and used for cloning cDNAs by the RT-PCR technique from Solanum chacoense. One clone in which the primer was immediately followed by sequences corresponding to the remaining part of the conserved domain was obtained. A leaf cDNA and a genomic library were constructed from S. chacoense. Clones homologous to the PCR fragment were isolated by plaque hybridization from both libraries (CYPs.ch-1 and CYPs.ch-2, respectively). Based on DNA sequence analysis, the selected clones are 87.6% identical and belong to the CYP71 family. The CYPs.ch genes are present in multiple copies in the S. chacoense as well as in the S. tuberosum genome with some polymorphisms. The CYPs.ch transcripts are slightly induced by methyl jasmonate and abscisic acid in S. chacoense foliage.
Jahanfar, S, Eden, JA, Nguyen, T, Wang, XL & Wilcken, DEL 1997, 'A twin study of polycystic ovary syndrome and lipids', Gynecological Endocrinology, vol. 11, no. 2, pp. 111-117.
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Jung, BP, Nguyen, T, Kolakowski, LF, Lynch, KR, Heng, HHQ, George, SR & O'Dowd, BF 1997, 'Discovery of a Novel Human G Protein-Coupled Receptor Gene (GPR25) Located on Chromosome 1', Biochemical and Biophysical Research Communications, vol. 230, no. 1, pp. 69-72.
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We amplified human genomic DNA by the polymerase chain reaction (PCR) using oligonucleotides based on the primary sequence of the genes encoding the somatostatin receptors (SSTR) and the somatostatin-like receptor gene SLC-1. One resultant DNA fragment was used to screen a genomic DNA library resulting in the isolation of a gene, GPR25, encoding an additional member of the G protein-coupled receptor family (GPCR). GPR25 is intronless throughout its open reading frame (ORF) and encodes a protein of 360 amino acids. The receptor encoded by GPR25 shares highest identity to the receptor encoded by GPR15, angiotensin II type 1A receptor, and somatostatin receptor 5. Northern analysis found no transcripts expressed in liver or any of the 12 brain regions analyzed. Fluorescence in situ hybridization analysis localized GPR25 to chromosome lq32.1.
Lapsys, KM, Furler, SM, Moore, KR, Kguyen, TV, Herzog, H, Howard, G, Samaras, K, Carey, DG, Morrison, KA, Eisman, JA & Chisholm, DJ 1997, 'Relationship of a Novel Polymorphic Marker Near the Human Obese (OB) Gene to Fat Mass in Healthy Women', Obesity Research, vol. 5, no. 5, pp. 430-433.
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AbstractLAPSYS, NM, SM FURLER, KR MOORE, TV NGUYEN, H HERZOG, G HOWARD, K SAMARAS, DG CAREY, NA MORRISON, JA EISMAN, DJ CHISHOLM. Relationship of a novel polymorphic marker near the human obese (OB) gene to fat mass in healthy women.The cloning of the murine obese (ob)gene and its human homologue has recently been reported. Mutations in the mouse obgene result in hereditary obesity; however, the role of variations of OBin the regulation of bodyweight in humans has yet to be determined. The contribution of putative genetic variations in the human OBgene to total and regional fat mass in a normal twin population has been analyzed through linkage and association with a novel polymorphic marker, located in proximity to this gene. The polymorphic dinucleotide repeat, isolated from a PI clone containing the human OB gene, was physically localized by long‐range restriction mapping to within 30 kilobases of the OB locus. The marker was genotyped in a population of 47 healthy female/female dizygotic (DZ) twin pairs for which direct measures of central abdominal and whole body fat had been obtained by dual X‐ray absorbtiometry. Possible linkage between the microsatellite marker and whole‐body (p=0.008), but not central abdominal (p=0.09), fat deposits was indicated. No association between fat depot phenotype and marker genotype was detected. These results suggest that genetic variation in or close to the human OB gene may play a role in the size of body fat stores in healthy women.
Morrison, NA, Qi, JC, Tokita, A, Kelly, PJ, Crofts, L, Nguyen, TV, Sambrook, PN & Eisman, JA 1997, 'Correction: Prediction of bone density from vitamin D raceptor alleles', Nature, vol. 387, no. 6628, pp. 106-106.
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Nguyen, TV, Sambrook, PN & Eisman, JA 1997, 'Sources of Variability in Bone Mineral Density Measurements: Implications for Study Design and Analysis of Bone Loss', Journal of Bone and Mineral Research, vol. 12, no. 1, pp. 124-135.
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Abstract Measurement of bone mineral density (BMD) is a useful tool for monitoring efficacy in osteoporosis therapy. However, the ability to detect true change for a subject as well as for a group of subjects is dependent on the precision of the measurement. In this paper, short-term and long-term reliability of bone mass measurements were examined at the spine and femoral neck using dual-photon and dual-energy X-ray absorptiometry and related to guidelines for study design. The concepts involved in these analyses are relevant to a study for any therapy involving a quantitative trait. Short-term reliability was assessed by repeated measures in 60 subjects aged 46 ± 9 years (mean ± standard deviation [SD]), and in 32 elderly subjects (aged 75 ± 5 years), on the same day with repositioning. Long-term variability in the rate of linear changes in BMD was assessed in a cohort of 293 women and 184 men, aged 60+, each having BMD measured on three separate occasions over an average interval of 2 years. Short-term variability in BMD was assessed using the coefficient of reliability (R) and standard deviation (SD) of measurement error. Long-term variability in BMD was modeled by linear regression. In the younger sample, the SD of measurement error for the lumbar spine and femoral neck was 14 and 25 mg/cm2, respectively, yielding coefficients of reliability for short-term measurements of 0.99 and 0.97, respectively. In the elderly sample, the coefficient of reliability was 0.96 and 0.77 for lumbar spine and femoral neck, respectively. For long-term variability, for which a linear rate of change in BMD was assumed, the SD of intrasubject variation in the women was 42 mg/cm2 at both the lumbar spine and femoral neck and in men 57 and 42 mg/cm2, respectively. The between-subject SD of the rates of change was higher in males than females (21 and 14 mg/cm2/year, respectively; p = 0.037). Importantly, intrasubject estimati...
O'Dowd, BF, Nguyen, T, Jung, BP, Marchese, A, Cheng, R, Heng, HHQ, Kolakowski, LF, Lynch, KR & George, SR 1997, 'Cloning and chromosomal mapping of four putative novel human G-protein-coupled receptor genes', Gene, vol. 187, no. 1, pp. 75-81.
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We report the discovery of four novel human putative G-protein-coupled receptor (GPCR) genes. Gene GPR20 was isolated by amplifying genomic DNA with oligos based on the opioid and somatostatin related receptor genes and subsequent screening of a genomic library. Also, using our customized search procedure of a database of expressed sequence tags (dbEST), cDNA sequences that partially encoded novel GPCRs were identified. These cDNA fragments were obtained and used to screen a genomic library to isolate the full-length coding region of the genes. This resulted in the isolation of genes GPR21, GPR22 and GPR23. The four encoded receptors share significant identity to each other and to other members of the receptor family. Northern blot analysis revealed expression of GPR20 and GPR22 in several human brain regions while GPR20 expression was detected also in liver. Fluorescence in situ hybridization (FISH) was used to map GPR20 to chromosome 8q, region 24.3-24.2, GPR21 to chromosome 9, region q33, GPR22 to chromosome 7, region q22-q31.1, and GPR23 to chromosome X, region q13-q21.1.
Samaras, K, Spector, TD, Nguyen, TV, Baan, K, Campbell, LV & Kelly, PJ 1997, 'Independent genetic factors determine the amount and distribution of fat in women after the menopause.', J Clin Endocrinol Metab, vol. 82, no. 3, pp. 781-785.
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Central adiposity is a strong predictor of cardiovascular disease in women. We studied postmenopausal twins to explore the strength and the relationship between genetic influences on body fat and its distribution in a group where cardiovascular disease is the major cause of mortality. Healthy twin women were recruited from a national media campaign. One hundred nineteen monozygotic (MZ) and 97 dizygotic twin pairs were studied (mean +/- SE age 60 +/- 0.3 yr; 10 +/- 0.4 yr post menopausal). Total and central body fat were measured by dual-energy x-ray absorptiometry. Intrapair resemblance was significantly greater in MZ pairs for total fat (MZ vs. dizygotic, r = 0.70 +/- 0.05 vs. r = 0.46 +/- 0.08, P = 0.005) and central fat (r = 0.62 +/- 0.06 vs. r = 0.35 +/- 0.09, P = 0.005), suggesting a strong genetic influence on these traits. Model-fitting analysis indicated that genetic factors contribute up to 60% of total population variance in both total and central body fat. The heritability of central fat remained, after adjustment for the heritability of total fat, suggesting an independent genetic influence on fat distribution. These results were unchanged after adjusting for the effects of estrogen replacement and smoking. In conclusion, total adiposity and central abdominal fat mass in normal postmenopausal women are under strong genetic influence. The data suggest that some of the genes responsible for central adiposity and its metabolic sequelae will be different from those responsible for total adiposity.
Sawzdargo, M, George, SR, Nguyen, T, Xu, S, Kolakowski, LF & O'dowd, BF 1997, 'A Cluster of Four Novel Human G Protein-Coupled Receptor Genes Occurring in Close Proximity to CD22 Gene on Chromosome 19q13.1', Biochemical and Biophysical Research Communications, vol. 239, no. 2, pp. 543-547.
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In our search for novel human galanin receptor (GALR) subtypes, human genomic DNA was PCR amplified using sets of degenerate primers based on conserved sequences in human and rat GALR. The sequence of one of the subcloned PCR products revealed homology to a sequence in the 3' region of the human CD22 gene following a BLAST search of GenBank's database. A search for open reading frames (ORF) in the non-coding CD22 sequence resulted in identification of two novel putative intronless genes, GPR40 and GPR41. The recent submission of sequence overlapping the downstream CD22 sequence revealed a possible polymorphic insert containing a third intronless gene, GPR42, sharing 98% amino acid identity with GPR41, followed by a fourth intronless gene, GPR43. Thus, the GPR40, GPR41, GPR42, and GPR43 genes, respectively, occur downstream from CD22, a gene previously localized on chromosome 19q13.1. The four putative novel human genes encode new members of the GPCR family and share little homology with GALR.
