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Biomedical subjects

P Harley

Publications and source records attributed to P Harley.

8 recordsLinked to original sources

A goniometric glove for clinical hand assessment. Construction, calibration and validation.

The construction of a goniometric glove is described. Each of the sensors in the glove was calibrated over a custom built metal hand using blocks of known angles as angular references. The digital data output from each sensor of the glove were converted into angular displacements at each joint. The glove was validated for consistency of measurement and accuracy over a custom built metal jig and in the human hand. The accuracy of the glove was found to be within the limits of traditional goniometry. It is proposed that goniometric gloves could be useful in the assessment of hand function.

Calibration↗

Virtual arthroscopy training: do the "virtual skills" developed match the real skills required?

The purpose of the study is to validate the training efficacy of the PC-based Sheffield Knee Arthroscopy Training System (SKATS, as described in MMVR6). Based on a task analysis of real arthroscopy, an evaluation module has been designed to test the core psycho-motor skills used in arthroscopy. The evaluation simulates a joint inspection and triangulation task, which is used to assess the research hypothesis that experienced arthroscopists will perform significantly better on the virtual arthroscopy simulator, than a trainee arthroscopist group and a control group. A group of experienced arthroscopic knee surgeons, a trainee surgeon group and a control group were tested on the simulator. The preliminary results indicate that experienced surgeons performed best with fewer instrument collisions and faster task-completion times. The results indicate that the core skills of arthroscopy used on the SKATS simulator are similar to those used in real arthroscopy. Further validation work is required to assess the training transfer effects. Once the simulator has been validated fully, it may prove beneficial in minimising patient risk.

Arthroscopy↗

Environmental controls over isoprene emission in deciduous oak canopies.

In summer 1992, isoprene emission was measured on intact leaves and branches of Quercus alba (L.) at two heights in a forest canopy. Isoprene emission capacity (measured at 30 degrees C and a photosynthetic photon flux density of 1000 micro mol m(-2) s(-1)) was significantly higher in sun leaves than in shade leaves when expressed on a leaf area basis (51 versus 31 nmol m(-2) s(-1); P < 0.01). Because leaf mass per unit area (LMA, g m(-2)) was higher in sun leaves than in shade leaves, emissions of sun and shade leaves expressed on a dry mass basis did not differ significantly (99 versus 89 micro g C g(DW) (-1) h(-1); P = 0.05). Similar measurements in 1995 were consistent with the 1992 data, but data from leaves in more shaded locations demonstrated that isoprene emission capacity decreased with decreasing growth irradiance, irrespective of units of expression. Isoprene emission capacity in leaves of Q. coccinea Muenchh. and Q. velutina Lam. also declined steeply with canopy depth. Emission capacity, on a dry mass basis, showed no obvious pattern with canopy position in Q. prinus L. There was no difference in the temperature response of sun versus shade leaves of Q. alba, but shade leaves exhibited a greater quantum efficiency and saturated at lower irradiance than sun leaves. Rates of isoprene emission measured on branches of Q. alba were approximately 60% of those measured on individual leaves, as a result of self-shading within branch enclosures. It is recommended that within-canopy variation in isoprene emission capacity be incorporated into regional emission models.

Journal Article↗

Fatty acids mediate the acute extrahepatic effects of insulin on hepatic glucose production in humans.

We have shown previously in humans that insulin partly suppresses hepatic glucose production (HGP) by an extrahepatic (indirect) mechanism. In the present study, we investigated the role of free fatty acids (FFAs) in mediating the extrahepatic effects of insulin in humans and determined the extent to which insulin can regulate HGP by a non-FFA-mediated effect. Sixteen healthy men received an intravenous tolbutamide infusion for 3 h, and pancreatic insulin secretion was calculated by deconvolution of peripheral C-peptide levels. On a subsequent occasion, equimolar exogenous insulin was infused by peripheral vein. In both studies, glucose was clamped at euglycemia. We have previously validated this method and shown no independent insulin-like activity of tolbutamide. During the clamp, 9 of the 16 subjects received a low dose of heparin and Intralipid to prevent the insulin-induced suppression of FFAs, while 7 subjects received a high dose of heparin and Intralipid to raise FFAs approximately 2.5-fold. In both the high- and low-dose groups, peripheral insulin was higher and calculated portal insulin lower with peripheral versus portal insulin delivery. In the low-dose group, HGP decreased by 68.3 +/- 2.1% with portal insulin delivery and 64.7 +/- 3.7% with peripheral insulin delivery (NS). In the high-dose group, HGP decreased by 58.0 +/- 4.5% with portal insulin and 48.3 +/- 5.0% with peripheral insulin (P < 0.05). Four individuals who participated in the high-dose group underwent an additional peripheral insulin study in which the same dose of exogenous insulin was infused as in the high-dose group but in the absence of heparin and Intralipid. During this latter study, FFA levels declined by approximately 90% during hyperinsulinemia, and HGP was suppressed by 71.8 +/- 5.6%, which was a much greater suppression (P < 0.01) than when FFA levels were raised in these subjects during the equivalent rate insulin infusion. In summary, the previously observed greater suppression of HGP with equimolar peripheral versus portal insulin is eliminated or reversed, depending on plasma FFA levels, if FFAs are prevented from decreasing, suggesting an important role of FFAs in mediating the extrahepatic effects of insulin on HGP. However, the effect of FFA clamping is relatively small with a significant degree of suppression of HGP (by approximately 50%), which remains even when FFAs are elevated above basal levels, suggesting that in the physiological range FFAs only partially influence the suppression of HGP in humans. This suggests that other mechanisms, most likely hepatic, dominate the acute insulin-induced suppression of glucose production.

Adult↗

Smooth muscle contraction and release of histamine and slow-reacting substance of anaphylaxis in pulmonary tissues isolated from guinea pigs passively sensitized with IgG1 or IgE antibodies.

In previous studies, we have provided evidence that different Fc receptors mediate antigen-induced pulmonary smooth muscle contractile responses after passive sensitization of guinea pigs with IgG1 or IgE antibodies. In this study, we examined the relationship between contraction and release of histamine and slow-reacting substance of anaphylaxis (leukotrienes) in superfused trachea and parenchymal strips as well as mediator release from minced lung fragments after passive sensitization of guinea pigs with IgG1 or IgE antibodies. Guinea pigs were immunized to produce either IgG1 or IgG1 and IgE using oxazolone-guinea-pig albumin or oxazolone-Ascaris plus cyclophosphamide, respectively. The contaminating IgG1 in the IgE-rich serum was removed by passage over a protein A-Sepharose column. Normal guinea pigs were passively sensitized intraperitoneally or intravenously with injections of either IgG1 or IgE 1 or 2 days before in vitro studies. Superfused tissues were challenged with 10(-1) mg/ml antigen (oxazolone-human serum albumin conjugate), and contractions and histamine and leukotriene release were monitored at discrete time intervals thereafter. At equivalent levels of contraction, substantially more histamine and leukotrienes were released from tissues taken from IgG1-sensitized animals. The amounts of histamine released from lung parenchymal strips and trachea in the IgE-sensitized state were approximately 5 and 38%, respectively, of those released from corresponding tissues in the IgG1-sensitized state. The leukotriene release from tissues isolated from IgE-sensitized animals was less than 4% of that released from tissues in the IgG1-sensitized state. Similar differences in mediator release were seen in comparable studies on minced lung fragments.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

Receptor-specific mediation by immunoglobulin E of antigen-induced contraction of tracheal and lung parenchymal strips isolated from the guinea pig.

The guinea pig is much like humans in the cells and mediators involved in immediate hypersensitivity reactions. However, the major anaphylactic antibody in this species is IgG1, not IgE. Recently, we have been successful in producing IgE antibody in guinea pigs. The current study examined whether guinea pig IgE antibody could mediate pulmonary smooth muscle contraction. IgE antibody to picryl and oxazolone determinants was induced by immunizing Hartley strain guinea pigs pretreated with cyclophosphamide. Hyperimmune serum from these animals was passed through a heavy chain-specific anti-IgG1 affinity column. The presence of IgE anti-hapten antibody in the filtrate fraction was verified by passive cutaneous anaphylaxis (PCA) testing with a 7-d period of local passive sensitization and by heat lability (56 degrees C X 4 h) of PCA activity. This IgE-rich fraction, and purified IgG1 anti-hapten antibody were transferred to normal guinea pigs. Both fractions sensitized trachea and pulmonary parenchyma for antigen-induced smooth muscle contraction. The IgG1-mediated antigen-induced contractile response was not affected by heat (56 degrees C X 4 h) and was inhibited in a dose-dependent fashion by IgG1 blocking antibody (anti-OA). The IgE-mediated antigen-induced contractile response was significantly decreased by heat and was not affected by the anti-OA blocking antibody even at a concentration of 100 mg/kg. Thus, two antigen-specific factors in guinea pig serum can mediate antigen-induced pulmonary smooth muscle contraction: IgG1 and IgE antibodies. Our data also suggests that these antibodies mediate the contractile response through separate receptors. The finding that guinea pig IgE can mediate pulmonary smooth muscle contraction suggests this species can be a model for IgE-mediated events in the lung.

Animals↗