PubMed Health⌕ Search

Biomedical subjects

A Temple

Publications and source records attributed to A Temple.

At least 19 recordsLinked to original sources
PubMed2004

Early analgesic effects of parecoxib versus ketorolac following laparoscopic sterilization: a randomized controlled trial.

BACKGROUND: The aim of this prospective double blind randomized controlled trial was to compare the effects of ketorolac and parecoxib on early postoperative pain. METHOD: We studied 36 ASA I/II patients who received a standardized general anaesthetic for laparoscopic sterilization. Patients were allocated randomly to receive either parecoxib 40 mg i.v. or ketorolac 30 mg i.v., at induction. After surgery, patients were assessed on awakening and then at 1, 2, and 3 h. Abdominal pain at rest and on inspiration, in addition to nausea and sedation were assessed on a 100 mm visual analogue scale. RESULTS: Of 36 patients, one was excluded from analysis. In the remaining patients, pain scores at rest and on inspiration were significantly lower in patients given ketorolac compared with those given parecoxib. This difference was attributable to the higher pain scores on awakening and at 1 h postoperatively in the parecoxib group compared with the ketorolac group. Despite this initial difference, there was no significant difference between the two groups in the number of patients receiving rescue analgesia. The median (interquartile range) time to consumption of rescue cocodamol of 60 (46-74) min in the parecoxib group was not significantly shorter than that of 100 (70-130) min in the ketorolac group. The amount of cyclizine given, nausea and sedation did not differ significantly between the groups. CONCLUSION: We found that parecoxib 40 mg i.v. given at induction of anaesthesia was less effective than or ketorolac 30 mg i.v., in the first hour after laparoscopic sterilization.

Adult↗
PubMed1997

Variation at the lipoprotein lipase and apolipoprotein AI-CIII gene loci are associated with fasting lipid and lipoprotein traits in a population sample from Iceland: interaction between genotype, gender, and smoking status.

The effects of polymorphisms in the lipoprotein lipase (LPL) gene (HindIII and S447X) and in the apolipoprotein (apo) AI-CIII gene cluster (G75A and C1100T) on levels of fasting plasma triglycerides, apoCIII, high density lipoprotein cholesterol (HDL-C), and apoAI were examined in 315 healthy men and women from Iceland. Non-smoking and smoking men and women were examined separately because of the strong effects of smoking status and gender on lipoproteins. For the LPL gene, there were no significant associations between plasma traits and genotypes of the S447X polymorphism, but the LPL-HindIII polymorphism was associated with significant effects on levels of all traits, with the effect of genotype on triglycerides and apoAI being modulated by smoking status, (genotype x smoking interaction, P < .02). The H- allele was generally associated with slightly lower levels of apoCIII, with a lowering effect on triglycerides only in smokers and with a raising effect on ApoAI in non-smoking and smoking men and in non-smoking women. For the apoCIII C1100T polymorphism, smoking and non-smoking men with one or more T alleles had levels of triglycerides roughly 10% higher than those with only the C allele; in contrast, the women with the T allele had lower levels of triglycerides (15.7% lower in non-smokers, P = .04; gender x genotype interaction, P = .02). In males and females and in smokers and non-smokers, the T allele was associated with levels of apoCIII that were 9-20% higher than those with only the C allele (P = .004 overall). In the non-smoking men, nonlinear additive effects were observed with combinations of genotypes at the LPL and apoAI-CIII loci, with the HDL-C and apoAI raising effect associated with the A75 allele and H- allele seen only in those men with both alleles, and the apoCIII raising effect associated with the H+ and T alleles seen only in those with both alleles. Thus, variations at both of the LPL and apoAI-apoCIII loci influence levels of triglycerides, apoCIII, HDL-C, and apoAI, but these effects are strongly modulated by smoking and are different between men and women. The mechanisms for these interactions between smoking or gender and genes are unknown, but future studies should take such interactions into account.

Adolescent↗
PubMed1996

Low plasma levels of factor VIIc and antigen are more strongly associated with the 10 base pair promoter (-323) insertion than the glutamine 353 variant.

In a group of 705 healthy middle-aged men, we have examined the relationship between plasma levels of Factor VII (FVII) c and Factor VII antigen (FVIIag) and two polymorphisms in the FVII gene. One polymorphism alters arginine at position 353 to glutamine (R/Q), and the other is the result of a 10 base pair (bp) insertion in the promoter region at position -323 from the start of translation (0/10bp). The frequency for the Q allele was 0.105 (95% CI 0.09-0.12) and for the 10bp allele was 0.117 (95% CI 0.10-0.13). Men who were carriers of either of the rare alleles had levels of FVIIc and FVIIag that were approximately 20% lower than non-carriers, and both of these effects were highly statistically significant (p < 0.0001). Strong allelic association was observed between the two polymorphisms, with R and 0 bp being on the same chromosome in 96% of cases, and Q and 10 bp being on the same chromosome in 90% of cases where this could be determined unambiguously (Delta = 0.92, chi 2 = 1206, p < 0.0001). This strong allelic association created three major genotype groups which were found to have significantly different levels of FVIIc (p < 0.001). In the 547 men homozygous for both common alleles (R/R & 0/0), mean (SD) FVIIc was 101 (29) as compared with 85 (30) in the 20 men with the genotype R/R & 0/10 and 81 (23) in the 126 men with the genotype R/Q & 0/10, suggesting a larger lowering effect associated with the 10 bp allele (16%) compared to the Q allele (an additional 4%). The lowering effect on FVII associated with the 10 bp allele remained statistically significant after adjusting for the effect of the Q allele (p = 0.004 for FVIIc and p = 0.06 for FVIIag), but the effect associated with the Q allele was no longer significant after adjusting for the 10 bp allele, suggesting that the strongest effect on levels of FVIIc was associated with the 0/10 bp genotype. In the sample overall, plasma FVIIc was associated positively with serum triglyceride concentration and the slope of this relationship was significantly greater in those with the genotype R/R compared to the other groups combined (0.12 versus 0.02, p = 0.008) with differences of similar size seen in the 0/0 compared to 0/10 + 10/10 groups. However, using the combined genotype, the slope of this relationship in the R/R & 0/10 group was 0.38 and was significantly steeper (p = 0.01) than in the other two groups who did not differ in this respect (slopes 0.11 and 0.08). This effect was seen on four subsequent annual examinations, and was also evident in the relationship between FVIIag and triglyceride concentration (p = 0.003 for difference between groups measured at baseline only). These data suggest that part of the previously described effects on FVIIc levels associated with the R/Q polymorphism may be explained by genetic variation in the promoter region of the FVII gene.

Antigens↗
PubMed1995

Genetic determination of coagulation factor VIIc levels among healthy middle-aged women.

A recent study (1) reported variation among men in clotting factor VIIc levels is associated with a genetic polymorphism detected by the restriction enzyme Msp I. The present study determined the Msp I genotype (Arg353, Gln353 alleles) for 189 women (mean age 53) who were subjects in the Healthy Women Study, a population study of CHD risk factor change at menopause. Women with the Arg/Arg genotype (n = 147) had an 16% higher (geometric) mean FVIIc level than those with the Arg/Gln (n = 41) genotype (1.21 vs 1.04 U/ml, p < 0.01), while the one subject with the Gln/Gln genotype had an FVIIc level of 1.00 U/ml. These results are consistent with those previously found in healthy men (1). In addition, women carrying the Gln allele did not exhibit the elevation in FVIIc with menopause and use of hormone therapy found among those with the Arg allele, suggesting that genotype may modify the observed rise in factor VIIc at menopause. Possibly because of the small sample size this interaction did not reach conventional levels of statistical significance. Results of multiple linear regression analyses controlling for age, hormone use, obesity, (ln) triglyceride levels, and family history of CHD found FVIIc levels to be significantly (p < 0.001) related to genotype. Thus, genotype appears to be a major determinant of FVIIc levels among women.

Adult↗
PubMed1992

Genetic factors determining thrombosis and fibrinolysis.

Raised plasma levels of fibrinogen, factor VIIc, and plasminogen activator inhibitor-1 (PAI-1) are associated with an increased risk of ischemic heart disease. Levels of these proteins are determined in part by environmental influences such as smoking and dietary fat intake. However, genetic variation explains much of the interindividual variation in plasma levels of these proteins not accounted for by environmental factors. We previously investigated the DNA variation at the fibrinogen gene locus and showed that BclI restriction fragment length polymorphism (RFLP) of the beta-fibrinogen gene is associated with between-person differences in plasma fibrinogen levels. This RFLP is unlikely to be the functional base change itself, since it lies downstream of the gene. The rate-limiting step in the production of the mature fibrinogen molecule in the human hepatoma cell-line HepG2 is the synthesis of the beta-polypeptide chain, which in turn is influenced by the amount of messenger (mRNA) available. One possibility is that BclI RFLP is in linkage disequilibrium with a base change in the region of the beta-gene controlling synthesis of its mRNA and ultimately of fibrinogen protein. We identified a base change in the 5'-flanking region of the beta-fibrinogen gene that is in linkage disequilibrium with the BclI RFLP, that is associated with plasma fibrinogen levels, and that may be involved in control of fibrinogen gene expression. For the factor VII gene, we identified a polymorphism, detected after Msp I digestion of polymerase chain reaction (PCR)-amplified genomic DNA, that is strongly associated with factor VII coagulant activity (factor VIIc). The base change that creates the Msp I polymorphism is a G to A substitution, leading to the replacement of arginine (Arg) with glutamine (Gln) in the protein product of the M2 allele. In a sample of 284 men from the United Kingdom the frequency of the Gln allele (M2 loss of cutting site) is 0.1, and individuals of genotype Arg/Gln have factor VIIc levels 22% below the sample mean. In this sample, the Msp I genotype was found to be the strongest predictor of factor VIIc, accounting for 20.2% of the variance, with cholesterol accounting for an additional 3.5%. Three individuals homozygous for the Gln allele had both low factor VIIc and low factor VII protein concentrations. The conformation of the factor VII Gln may be different from that of the Arg protein, affecting its intracellular processing, secretion, turnover in plasma, or activity.(ABSTRACT TRUNCATED AT 400 WORDS)

Factor VIII↗
PubMed1992

King's theory of goal attainment. Resolving filial caregiver role strain.

Although there is considerable literature on the types of problems encountered by caregivers, the problems faced by filial caregivers who are also health professionals has been overlooked. King's goal of nursing is to "help individuals maintain their health so they can function in their roles." Consequently, a misunderstanding of roles and distortion in perception, for whatever reason, may influence the outcome of care. King's theory provides nurses with a tangible and logical way of coping with the potentially debilitating effect of conflict between two roles or between two perceptions of a role.

Caregivers↗
PubMed1991

Expression of basement membrane proteins and interstitial collagens in dermal papillae of human hair follicles.

The expression of basement membrane molecules and interstitial collagens in human hair follicle mesenchyme was studied by immunohistochemical staining of tissue sections and of cells cultured from dermal papillae. Type I and type III collagens were found in the dermal sheath and in the dermal papilla throughout the hair cycle. Laminin and type IV collagen were expressed at the outer root sheath basement membrane and in the extracellular matrix of the dermal papilla of anagen and catagen follicles. In telogen follicles, where the volume of the dermal papilla extracellular matrix is much reduced, outline staining of dermal papilla cells for laminin and type IV collagen was still apparent. Staining for bullous pemphigoid antigen was also seen at the outer root sheath basement membrane extending to the lower tip of the hair bulb. In anagen follicles, there was no staining for bullous pemphigoid antigen at the interface between hair bulb epithelium and the dermal papilla and no staining within the dermal papilla. However, linear staining for bullous pemphigoid antigen became continuous around hair follicle epithelium during catagen and telogen. Cells cultured from human dermal papillae also stained for interstitial collagens, type IV collagen and laminin. However, similar results were obtained when cultured dermal fibroblasts were stained with the same antibodies. The expression of basement membrane proteins in human dermal papillae resembles that seen in follicles from other mammalian species and suggests that this is relevant to dermal papilla function. Cultured dermal papilla cells express a similar pattern of interstitial collagens and basement membrane proteins to those seen in tissue sections but this finding is not specific to dermal papilla cells.

Antibodies, Monoclonal↗
PubMed1991

Lipoid proteinosis--new immunopathological observations.

Lipoid proteinosis is described in a family of Scottish descent. Chromosome studies performed on five members were normal. Direct immunofluorescence studies performed on skin with anti-collagen antibodies showed an abnormal distribution of collagen within the skin. No abnormality was detected in DNA extracted from lymphocytes taken from five family members, when probed with gene probes to collagen types alpha 1 (I), alpha 2 (I), alpha 1 (III) and alpha 2 (V).

Adult↗
PubMed1988

A PvuII polymorphism in the 5' flanking region of the apolipoprotein AIV gene: its use to study genetic variation determining serum lipid and apolipoprotein concentration.

We have used a 1.05-kb unique genomic fragment from the 5' end of the apolipoprotein (apo) CIII gene to identify a restriction fragment length polymorphism (RFLP) detected with the restriction enzyme PvuII, in the apoCIII-apoAIV intergenic region. In a sample of 220 normolipidaemic individuals from the UK population, the frequency of the rare allele, VB2 is 0.054. The PvuII polymorphism is in apparent linkage equilibrium with three other RFLPs of this gene cluster, detected with the restriction enzymes XmnI, PstI and SstI, but in linkage disequilibrium with an RFLP in the apo-CIII gene also detected with PvuII. Taken together, these five RFLPs have a PIC (polymorphism information content) value of 0.8, and therefore are informative for genetic studies. Individuals with the genotype VB1VB2 had lower mean concentrations of apoAI, and HDL-cholesterol than individuals with the genotype VB1VB1. However these differences were not statistically significant.

Apolipoprotein C-III↗
PubMed1980

Cytolysis of fibroblasts by C3a.

C3a was found to be more cytolytic to transformed than to primary fibroblast cultures from mouse and man. Fibroblasts made quiescent with caffeine were lysed by the same concentrations of C3a as untreated cells. These findings may have implications in tumour immunity.

Animals↗
PubMed1980

Demonstration of transferrin receptors on human placental trophoblast.

It has been postulated that the transplacental passage of maternal iron to the developing fetus requires binding of maternal transferrin to the trophoblast. We have therefore examined the ability of the human placenta to bind transferrin in vitro. Transferrin was demonstrated on trophoblast of human chorionic villi by immunohistologic methods. Moreover, after removal of transferrin bound in vivo by treatment of tissue with chaotropic solution or phosphate-buffered saline, freshly added transferrin was shown to bind in vitro in the same characteristic distribution. These findings suggest that placental iron transport is initiated by uptake of maternal transferrin iron to specific trophoblast binding sites.

Albumins↗