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G Duff

Publications and source records attributed to G Duff.

16 recordsLinked to original sources
PubMed2000

Increased risk of fibrosing alveolitis associated with interleukin-1 receptor antagonist and tumor necrosis factor-alpha gene polymorphisms.

Fibrosing alveolitis (FA) is characterized by persistent inflammation and elevated production of tumor necrosis factor-alpha (TNF-alpha), interleukin-1 beta (IL-1beta), and interleukin-1 receptor antagonist (IL-1ra) in the lung. Single base variations at position +2018 in the IL-1ra gene (IL-1RN) and position -308 in the TNF-alpha gene (TNF-A) are overrepresented in other chronic inflammatory disease populations. We have tested the hypothesis that predisposition to FA may also be influenced by these polymorphisms by genotyping 88 cases and matched controls from England and 61 cases and 103 unmatched controls from Italy. The rarer allele for IL-1RN and TNF-A was designated allele 2 in each case. For IL-1RN allele 2, in the English group, the relative odds of FA were increased in homozygous subjects by an odds ratio (OR) of 10.2 (95% confidence intervals [CI], 1.26 to 81.4; p = 0.03) and for carriers by an OR of 1.85 (95% CI, 0.94 to 3.63; p = 0.075). In the Italian population, the risk of FA was increased, in IL-1RN allele 2 homozygotes (OR, 2.54; 95% CI, 0.68 to 9.50; p = 0.2) and in carriers (OR 2.40; 95% CI, 1.26 to 4.60; p = 0.008). Carriage of TNF-A allele 2 was also associated with increased risk of FA in the English (OR, 1.85; 95% CI, 0.94 to 3.63; p = 0.075) and Italian (OR, 2.50; 95% CI, 1.14 to 5.47; p = 0.022) populations. These data suggest IL-1RN (+2018) allele 2 and TNF-A (-308) allele 2 confer increased risk of developing FA and, therefore, that unopposed IL-1beta and/or excessive TNF-alpha may play a pathophysiologic role in this condition.

Aged↗
PubMed1999

Effect of ruminal glucose infusion on dry matter intake, urinary nitrogen composition, and serum metabolite and hormone profiles in Ewes.

Twelve 18-mo-old Debouillet ewes were used to determine the effect of ruminal glucose infusion on DMI, on urinary ammonium (NH4+) and urea N (UUN) concentrations, and on serum metabolite and hormone profiles. Ewes were limit-fed a 90% concentrate diet for 30 d, stratified by BW into three groups (average BW = 82.6+/-1.1 kg), and assigned randomly to receive 0, 5, or 10 g of glucose/kg of BW via esophageal intubation. Urine was collected hourly for 12 h and blood (jugular venipuncture) at 30-min intervals for 12 h. After 12 h, ewes were housed individually, allowed free access to the diet, and DMI was recorded for 5 d. Venous blood pH averaged 7.49, 7.48, and 7.48 at 0 h and decreased (linear [L], P < .01) at 12 h (7.41, 7.36, and 7.26) with increasing glucose. Serum glucose increased (L, P = .06) at 3 and 6 h. Serum L(+)-lactate increased (L, P = .08) at 3, 6, and 9 h, whereas serum D(-)-lactate increased linearly (P = .09) at 6 and 9 h and quadratically (P < .10) at 12 h. After the glucose challenge, DMI decreased (L, P < .05). Urinary pH and NH4+ were not influenced by glucose infusion; however, UUN increased at 3 (quadratic [Q], P < .05), 4, 5, 6 (L, P = .03), and 7 h (Q, P < .05) and decreased at 11 and 12 h (L, P = .09). As glucose infusion increased, serum creatinine increased at 9 (L, P < .01) and 12 h (Q, P = .02). Generally, serum Na and P increased (P = .09), whereas K decreased (P < .05), with glucose infusion. Lactate dehydrogenase activity increased with glucose infusion (Q, P < .10) at 3, 6, 9, and 12 h. Increasing glucose infusion increased serum globulin (Q, P = .06), albumin, and total protein (L, P = .08). Serum prolactin and vasopressin were not influenced (P = .22) by glucose infusion. Serum insulin and aldosterone increased quadratically (P = .08), whereas serum growth hormone decreased linearly (P = .08) as a result of increasing glucose infusion. Results suggest that UUN, serum insulin, aldosterone, and several serum constituents may serve as markers of organic acid load in ruminants fed high-concentrate diets.

Acidosis, Lactic↗
PubMed1998

Dating the origin of the CCR5-Delta32 AIDS-resistance allele by the coalescence of haplotypes.

The CCR5-Delta32 deletion obliterates the CCR5 chemokine and the human immunodeficiency virus (HIV)-1 coreceptor on lymphoid cells, leading to strong resistance against HIV-1 infection and AIDS. A genotype survey of 4,166 individuals revealed a cline of CCR5-Delta32 allele frequencies of 0%-14% across Eurasia, whereas the variant is absent among native African, American Indian, and East Asian ethnic groups. Haplotype analysis of 192 Caucasian chromosomes revealed strong linkage disequilibrium between CCR5 and two microsatellite loci. By use of coalescence theory to interpret modern haplotype genealogy, we estimate the origin of the CCR5-Delta32-containing ancestral haplotype to be approximately 700 years ago, with an estimated range of 275-1,875 years. The geographic cline of CCR5-Delta32 frequencies and its recent emergence are consistent with a historic strong selective event (e.g. , an epidemic of a pathogen that, like HIV-1, utilizes CCR5), driving its frequency upward in ancestral Caucasian populations.

Acquired Immunodeficiency Syndrome↗
PubMed1997

Using models in learning disability nursing.

Nursing models and theory can be of particular benefit during periods of significant social and professional change. The use of nursing models in learning disability nursing needs to be shown to have positive outcomes in practice. A literature search found little proof of the efficacy of nursing models in learning disability nursing. More nursing research is essential in this area of practice.

Evidence-Based Medicine↗
PubMed1995

Prenatal sonography for the detection of fetal anomalies: results of a prospective study and comparison with prior series.

OBJECTIVE: Reported rates of sonographic detection of fetal anomaly vary widely. The purpose of our study was to determine how well we were detecting fetal anomaly in our region and to compare our results with published series using standardized criteria. SUBJECTS AND METHODS: Over a 2-year period, we compared the reports of sonographic studies done in 7880 pregnancies at 16-20 weeks' gestation with all pregnancy outcomes established by medical records and pathologic results of the infants, whether born alive or dead. Fetal anomaly was defined as any structural anomaly except for those specifically excluded. We compared our results, expressed as percentage of anomalies found and anomalies found per 1000 pregnancies screened, with those of published studies, modifying published figures where necessary to compensate for our defined exclusion criteria. RESULTS: At postnatal examination, we found 157 anomalies in 144 babies who had prenatal sonography at 16-20 weeks' gestation. We detected 93 anomalies (60%) in 84 fetuses, leading to termination of pregnancy in 42 cases (50% of anomalous fetuses). The prevalence of fetal anomaly in our population was 19.8 anomalies per 1000 pregnancies screened. We detected 11.8 anomalies per 1000 screened, leading to termination of 5.3 pregnancies per 1000 screened. Our success rate for fetal anomaly detection ranged from 92% for CNS anomalies to 31% for cardiac anomalies and 25% for craniofacial anomalies. There were fewer babies born with a major malformation in the group whose anomalies were detected prenatally (21%) than in the group whose anomalies were not detected (58%). By comparison, in prior series, prevalence of anomalies varied from 5.67 to 25.95 per-11000 screened; anomaly detection varied from 16.6% to 74.4%; detection rate varied from 3.08 to 11.03 per 1000 screened. There was no correlation between the percentage and per 1000 detection rates. Thus, the RADIUS and Helsinki trials had similar detection rates per 1000, but more than a twofold difference in percentage detection rate. Similarly, the percentage success rate in studies could be the same, but the detection rate per 1000 different threshold. There was a similar lack of correlation for rates of pregnancy termination. All series except for the RADIUS study reported a reduction in the rate of adverse outcome if the anomalies were detected prenatally. CONCLUSION: Our rate of detection of fetal anomaly is satisfactory for most organ systems but remains poor for cardiac, skeletal, and craniofacial anomalies. The relative ranking of the success of fetal anomaly detection in prior studies depends on whether the detection rate is reported as a percentage or as the number of anomalies detected per 1000 screened. Our results compare favorably with those reported in other series.

Congenital Abnormalities↗
PubMed1993

Contrasting levels of in vitro cytokine production by rheumatoid synovial tissues demonstrating different patterns of mononuclear cell infiltration.

Synovial membrane samples obtained at knee arthroplasty from 22 patients with rheumatoid arthritis (RA) were characterized histologically. Two groups were identified. Tissue samples from 15 patients demonstrated multiple focal lymphoid aggregates of mononuclear cells (group A). Samples from the remaining seven patients demonstrated diffuse mononuclear cell infiltration (group B). Samples of each synovial membrane (0.25 g) were cultured for cytokine production. The highest levels of IL-1 beta and IL-6 were produced by group A tissues: 19.1 +/- 19.6 ng/ml IL-1 beta (mean +/- s.d.) and 264.4 +/- 301.9 ng/ml IL-6, versus 3.8 +/- 6.6 ng/ml and 54.7 +/- 42.6 ng/ml respectively. Small quantities of IL-2 and IL-4 were measured in both groups: the levels of IL-2 in group A cultures were highest (P = 0.04). Moreover, using MoAbs, the most intense cytokine staining in the tissues was detected in group A. Similar total numbers of each cell subpopulation and similar quantities of immunoglobulin and rheumatoid factor synthesis were measured in both groups. It is suggested that the presence of multiple focal lymphoid aggregates associated with higher levels of cytokine production observed in group A represent a greater degree of immunological activation, and may represent a subgroup of patients with a greater potential for articular destruction.

Adult↗
PubMed1990

Modulation of interleukin 1 beta gene expression using antisense phosphorothioate oligonucleotides.

The production of interleukin 1 beta (IL1 beta) in lipopolysaccharide (LPS) stimulated monocytes was inhibited by 98% using antisense phosphorothioate oligonucleotides complementary to the 5' untranslated and exon 6 regions of IL1 beta mRNA. A sense phosphorothioate oligonucleotide failed to inhibit IL1 beta production. The inhibition of IL1 beta synthesis was not due to reduced cell viability and [35S]methionine incorporation showed that it could not be accounted for by an overall inhibition in protein synthesis. Tumour necrosis factor (TNF) and IL1 alpha production was also inhibited but to a lesser extent than IL1 beta. The use of antisense phosphorothioate oligonucleotides to inhibit IL1 production should enable the complex pathways of IL1 regulation to be elucidated and provide information on the biological role of these cytokines.

Base Sequence↗
PubMedDate not supplied

Respite choice.

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Child Behavior Disorders↗