Effect of frequent prenatal ultrasound on birthweight: follow up at 1 year of age. Western Australian Pregnancy Cohort (Raine) Working Group.
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Biomedical subjects
Publications and source records attributed to S Evans.
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The objective of this study was to evaluate and characterise by study of newborn biometry a possible effect on birthweight which we observed previously in a randomised controlled trial of multiple prenatal ultrasound examinations. A total of 2743 women with single pregnancies had been allocated at random to either a protocol of ultrasound imaging and continuous wave Doppler studies at 18, 24, 28, 34 and 38 weeks gestation (intensive group), or to a protocol of a single imaging examination at 18 weeks and further imaging scans only as clinically indicated (regular group). When compared with those in the regular group, and adjusted for other confounding variables, normally formed babies of term gestational age in the intensive group tended to be shorter when measured at birth (P = 0.123) and on day 2-3 of age (P = 0.068). There were statistically insignificant reductions in the circumferences of the chest, abdomen and mid-arm; and in the skinfold thicknesses of the triceps, parascapular and subscapular regions. Principal component analysis showed a trend for a reduction for the skeletal component (P = 0.085) but not for the soft tissue component (P = 0.332). Comparison of the neonatal biometry in the two groups is not conclusive, but the differential effects on the various growth parameters suggest that if multiple scans do indeed restrict fetal growth, the mechanism is more likely to be an effect on bone growth rather than a reduction in nutrient supply from the placenta.
The diagnosis of idiopathic immune thrombocytopenia remains a clinical diagnosis based on the exclusion of other causes of immune and nonimmune thrombocytopenia. Measurement of platelet-associated Ig (PAIg), while sensitive, is nonspecific for the diagnosis of immune thrombocytopenia. Published experience of antigen capture assays (including monoclonal antibody immobilization of platelet antigens or MAIPA) suggest a high sensitivity and specificity (70% to 80%) in selected groups of patients. In a prospective evaluation of 158 patients with thrombocytopenia from all causes, we report a sensitivity of 51% and specificity of 80% for direct MAIPA assays. MAIPA was considerably better in discriminating immune from nonimmune thrombocytopenia than two assays of PAIgG. Antiplatelet antibodies detected by MAIPA were more frequently directed against the glycoprotein (GP) IIb/IIIa than the GP Ib/IX complex. Our experience suggests that MAIPA assays are useful in the laboratory assessment of thrombocytopenia, should be performed before therapy, and that some patients with 'nonimmune' thrombocytopenia may have genuine antiplatelet antibodies.
430 patients participating in the DSM-IV field trial receiving a DSM-III-R SCID-derived diagnosis of episodic major depression (n = 131), dysthymic disorder (n = 37) and double depression (n = 262) completed the social adjustment scale-self-report (Weissman and Bothwell, 1976). Patients with double depression demonstrated greater social morbidity than those suffering from episodic major depression or dysthymic disorder (P < 0.05). Significant predictors of high social morbidity in double depressives included severity of symptoms (P < 0.0001), followed by age of onset of first major depression (P < 0.04). Subscale analysis revealed that double depressives were significantly more impaired in work outside the home and in terms of their financial status (P < 0.05).
Previous studies suggested that the cross-reactivity rates of low molecular weight (LMW) heparins with the antibody in heparin-induced thrombocytopenia (HIT) are more than 80%, whilst that of the LMW heparinoid (Orgaran) is relatively low at about 10%. These earlier studies were limited either in the number of patients studied, or in investigating only a single drug. They were also inadequate due to non-standardisation of testing conditions. This study compares three LMW heparins (Fragmin, Clexane, Fraxiparin) and a heparinoid (Orgaran) in their cross-reactivity rates with the HIT antibody. The sera of 45 HIT patients were tested using platelet aggregometry under standardised conditions. The cross-reactivity rates are: 7% (Orgaran), 89% (Fragmin), 83% (Clexane) and 86% (Fraxiparin). Although there are no controlled trials to determine the in vivo cross-reactivity rates of LMW heparins and heparinoid, the low in vitro cross-reactivity rate of the latter favours its use in HIT. Nevertheless, the therapeutic use of these drugs in HIT should be preceded by exclusion of in vitro cross-reactivity.
Transplant renal artery stenosis (TRAS) is a common complication after transplantation and is an important cause of graft dysfunction. Damage from graft rejection, trauma, and atherosclerosis have been implicated as possible causes. We reviewed all 917 patients transplanted in our unit since 1978 to study the prevalence, clinical features, and possible causes of TRAS. Seventy-seven patients with TRAS were identified. The detected incidence was 2.4% before the introduction of color doppler ultrasonography (CDU) and rose to 12.4% after CDU was introduced in 1985, giving an overall incidence of 8.4% during a mean follow-up period of 6.9 years. The TRAS group was compared with a control group of 77 transplanted patients matched for age, year of transplant, sex, and number of previous grafts. Mean ages for the study and control groups were 43.6 +/- 15 and 44.8 +/- 13.7 yr. A total of 25% of cases of TRAS were diagnosed within the first 8 wk of transplantation and in 60% within the first 30 wk (median = 23 wk). All patients were treated with angioplasty, 28 patients had recurrence of TRAS requiring multiple angioplasties (maximum 5) and 1 went on to have surgery. Angioplasty resulted in a significant fall in plasma creatinine. Patient and graft survival were significantly worse in the TRAS group: 69% vs. 83% (P < 0.05) and 56% vs. 74% (P < 0.05) (TRAS vs. Control), respectively. There was a significantly higher incidence of rejection, especially cellular rejection in the TRAS group, 0.67 vs. 0.35 episodes per patient (P < 0.01) (TRAS vs. Control). Recurrence but not occurrence of TRAS was associated with the use of cyclosporine.
Twenty volunteers were trained to discriminate between 75 mg tripelennamine (TP) and placebo. During the first four sessions, the drugs were identified prior to ingestion by letter code. During the next six sessions, the procedure was the same except the capsules were not identified. At the end of the 3-h session, participants indicated which capsule they believed they received using the letter codes. When correct, they received a monetary bonus. If they were correct on five sessions, they entered the third phase which had ten additional training and 12 test sessions. During tests, participants received capsules that contained other drugs, including diphenhydramine (50 and 75 mg), chlorpheniramine (4 and 6 mg), diazepam (5 and 10 mg), d-amphetamine (5 and 10 mg), as well as tripelennamine (25, 50 and 75 mg) and placebo. Thirteen participants learned the discrimination and nine entered the third phase. Except for placebo, most participants identified the test compounds as TP and labeled them as sedatives. TP produced significant changes on several subjective and physiological measures. The test compounds produced varied effects which were neither clearly dose-related nor related to the identification as TP or placebo. These results indicate that tripelennamine can function as a discriminative stimulus, but with little evidence of pharmacological specificity.
OBJECTIVE: To investigate erythrocyte membrane Na+, K(+)- and Ca2+, Mg(2+)-ATPase activities in newly diagnosed hypertensive patients before and after 2, 4, and 6 months of treatment with enalapril or captopril as monotherapy. METHODS AND RESULTS: Na+, K(+)-ATPase activity (nmol ATP hydrolysed/min per mg protein) rose by 6 months of treatment in both groups when values were compared in each treated group over time (4.5 +/- 0.8 to 9.9 +/- 1.2; 4.9 +/- 0.8 to 10.5 +/- 1.7, respectively, p < 0.001 for both). When the treated groups were compared with controls at each period of time, Na+, K(+)-ATPase activity was higher at months 4 and 6 (p < 0.001) for both groups, respectively). Ca2+, Mg(2+)-ATPase activity (nmol ATP hydrolyzed/min per milligram protein) in the absence and in the presence of calmodulin increased in the enalapril (6.4 +/- 0.7 to 8.9 +/- 0.95, p < 0.05; 13.4 +/- 1.2 to 17.2 +/- 1.2, p < 0.05, respectively) and captopril (7.0 +/- 0.6 to 8.5 +/- 0.7; 14.4 +/- 1.1 to 16.0 +/- 1.0, p < 0.05, respectively) groups after 6 months of treatment compared within each treated group over time. When patient groups were compared with controls at time 0, 2, 4, and 6 months, the pump activity was higher in the treated groups at 6 months. CONCLUSION: The long-term enhancement of cell membrane Na+, K(+)-and Ca2+, Mg(2+)-ATPase activity associated with enalapril and captopril therapy may represent a specific effect of these agents or alternatively, a nonspecific outcome of blood pressure reduction.
A technique for subtyping Campylobacter jejuni isolates has been developed by using the restriction fragment length polymorphism (RFLP) of polymerase chain reaction (PCR) products of the flaA and flaB genes. The technique was validated by using strains representing 28 serotypes of C jejuni and it may also be applied to C coli. From these strains 12 distinct RFLP profiles were observed but there was no direct relationship between the RFLP profile and the serotype. One hundred and thirty-five campylobacter isolates from 15 geographically distinct broiler flocks were investigated. All the isolates could be subtyped by using the RFLP method. Isolates from most of the flocks had a single RFLP profile despite data indicating that several serotypes were involved. Although it is possible that further restriction analysis may have demonstrated profile variations in these strains, it is more likely that antigenic variation can occur within genotypically related campylobacters. As a result, serotyping may give conflicting information for veterinary epidemiological purposes. This RFLP typing scheme appears to provide a suitable tool for the investigation of the sources and routes of transmission of campylobacters in chickens.
The dielectric properties of glycerol, propylene glycol, ethylene glycol and dimethyl sulphoxide have been measured in various aqueous concentrations generally sufficient to allow supercooling rather than freezing. The temperature range investigated is from -80 degrees C to +20 degrees C and the frequency range is 100 MHz to 2 GHz. The aim is to find the materials and conditions most favorable for very rapid re-warming of perfused biological tissue by electromagnetic fields, avoiding thermal runaway in the bulk and local non-uniformity of temperature. Frequencies below 500 MHz are generally indicated.
Enteral glutamine feeding effect on renal glutamine utilization was assessed from the perspective of gamma glutamyltransferase activity-dependent cellular glutamate modulation of phosphate-dependent glutaminase. After 4d, rats fed an elemental diet supplemented with glutamine exhibited a 2 1 % higher kidney glutamate content and 27% reduction in ammonium excretion, both P < 0.05. Glutamine removal from plasma was depressed 62% in the glutamine-fed group (324 +/- 155 vs. 780 +/- 154 nmol x min(-1) x 100 g body weight (-1), P < 0.05) despite an elevated arterial plasma glutamine load delivered to the kidney. Administration of acivicin, 36 mg/kg body weight, to glutamine-fed rats inhibited gamma glutamyltransferase > 90% and decreased kidney glutamate content 42%. This reduction in kidney glutamate was associated with a 3.3-fold enhancement in both glutamine extraction (474 +/- 184 to 1548 +/- 255 nmol x min(-1) x 100 g body weight (-1)) and ammonium excretion (295 +/- 30 to 978 +/- 96 nmol x min(-1) x 100 g body weight(-1)), both P < 0.01. These findings are consistent with enteral glutamine regulation of renal glutamine utilization through an elevation of the cellular glutamate level.
OBJECTIVE: To ascertain the demographic, pregnancy and obstetric factors associated with the delivery of a liveborn very preterm infant ( < 33 weeks of gestation) and to investigate any differences in these factors between identifiable aetiological groups. DESIGN: Cohort analytical study. SETTING: King Edward Memorial Hospital for Women (KEMH), Western Australia. MAIN VARIABLES EXAMINED: Maternal demographic and obstetric history, primary complication associated with delivery, obstetric management and mode of delivery. RESULTS: Six hundred and eight women who were delivered of 693 liveborn very preterm infants in Western Australia between 1.1.90 and 31.12.91, representing 1.22% of all women who were delivered of a liveborn infant in those years. Singleton pregnancy occurred in 517 (85%) and 541 (89%) were delivered in KEMH. Mean maternal age was 28 years with an excess of mothers less than 20 years of age and older than 34 years compared with the statewide perinatal data. Pre-eclampsia (n = 128, 21.1%), preterm prelabour rupture of membranes (n = 148, 24.3%), idiopathic preterm labour (n = 195, 30.4%) and antepartum haemorrhage (n = 111, 18.3%) were associated with 94.1% of deliveries. These proportions varied with plurality and period of gestation. Demographic details, use of antenatal steroids, exposure to labour and caesarean section delivery differed between mothers depending on the primary complication. Overall 322 (53.0%) received antenatal steroids and 297 (48.8%) were delivered by caesarean section. Factors associated with decreased use of steroids were gestational age of less than 27 weeks (odds ratio (OR) 0.54; 95% CI 0.36-0.83), preterm prelabour rupture of the membranes (OR 0.48; 95% CI 0.29-0.78) and idiopathic preterm labour (OR 0.56; 95% CI 0.35-0.91). Factors associated with increased use of steroids were multiple pregnancy (OR 1.70; 95% CI 1.02-2.81) and pre-eclampsia (OR 1.87; 95% CI 1.09-3.19). CONCLUSIONS: These very preterm deliveries account for only a small proportion of all deliveries. There are differences in the mother's demographic history, obstetric management and delivery depending on the primary aetiological factor.
OBJECTIVE: To ascertain the growth characteristics, delivery room management and hospital mortality of very preterm liveborn infants (< 33 weeks of gestation) and to identify differences between infants associated with the aetiological factor related to their very preterm delivery. DESIGN: Cohort analytical study. SETTING: King Edward Memorial Hospital for Women, Western Australia. MAIN VARIABLES EXAMINED: Gestational age, birthweight, birthweight ratio, condition at birth and mortality. RESULTS: Six hundred and ninety-three liveborn very preterm infants were born to 608 mothers between 1.1.90 and 31.12.91. This was 1.37% of all liveborns in Western Australia. Three hundred and eighty-five (55.6%) were male. Growth characteristics (birthweight, birthweight ratio and proportion small for gestational age) differed between infants depending on the primary obstetric complication associated with the very preterm delivery. Overall 217 (31%) infants were small for gestational age, 34(4.9%) had a congenital anomaly, and 102 (14.7%) died. Corrected mortality, excluding major fatal congenital anomaly, was 86 (12.7%). The majority of infants died on the first day (n = 59 (57.8%)). The only factors associated with an increased or decreased mortality were decreasing gestation (adjusted odds ratio (AOR) 1.7, 95% CI 1.50-1.93), decreasing birthweight ratio (small for gestational age) (AOR 1.3, 95% CI 1.08-1.53), antepartum haemorrhage as primary complication (AOR 3.1, 95% CI 1.25-7.69) and any antenatal steroids (AOR 0.26, 95% CI 0.14-0.51). In comparison with other studies, survival in the extremely preterm group, defined as a gestational age of less than 28 weeks, is improving. CONCLUSIONS: Very preterm infants account for a large proportion of perinatal mortality. Further studies are required to explore the differences between infants on the basis of the primary obstetric complication and to ensure that increased survival is not associated with an increase in disabilities.
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Methods to examine sputum for indices of airway inflammation are evolving. We have examined the repeatability and the validity of an improved method to measure sputum cells and fluid-phase eosinophil cationic protein (ECP), major basic protein (MBP), eosinophil-derived neurotoxin (EDN), albumin, fibrinogen, tryptase, and interleukin-5 (IL-5). Sputum was induced with hypertonic saline twice within 6 d in 10 healthy subjects, 19 stable asthmatics, and 10 smokers with nonobstructive bronchitis. The method included the processing of freshly expectorated sputum separated from saliva, treatment with a fixed proportion of dithiothreitol 0.1% followed by Dulbecco's phosphate-buffered saline, making cytospins, and collecting the supernatant. The reproducibility of measurements, calculated by the intraclass correlation coefficient, was high for all indices measured with the exception of total cell counts and proportion of lymphocytes. Asthmatics, in comparison with healthy subjects and smokers with bronchitis, had a higher proportion of sputum eosinophils (median percent 5.2 versus 0.5 and 0.3), metachromatic cells (0.3 versus 0.07 and 0.08), ECP (1,040 micrograms/L versus 288 and 352), MBP (1,176 micrograms/L versus 304 and 160), and EDN (1,512 micrograms/L versus 448 and 272). Asthmatics differed from healthy subjects, but not from smokers with bronchitis, in the proportion of neutrophils (46.9% versus 24.1%), albumin (704 versus 288 micrograms/mL), and fibrinogen (2,080 versus 440 ng/mL). Smokers with bronchitis showed a trend for a higher neutrophil count and levels of albumin and fibrinogen than healthy subjects. The proportion of sputum eosinophils correlated positively with ECP, MBP, EDN, albumin and fibrinogen levels, and metachromatic cell counts correlated with tryptase. In asthmatics, IL-5 correlated with eosinophil counts. There was a significant negative correlation between sputum indices and expiratory flows and methacholine PC20. Thus, the methods of measuring cell and fluid phase markers in induced sputum used in this study are reproducible and valid. They can therefore be used to reliably measure these indices of airway inflammation.
Inhalation of hypertonic saline to induce sputum may alter cells and fluid-phase markers in sputum. We have compared indices of inflammation in sputum produced spontaneously with sputum induced by an aerosol of hypertonic saline. Twenty-three asthmatics produced spontaneous followed by induced sputum on the same day. The sputum specimen was separated from saliva within 2 h, dispersed with dithiothreitol (DTT) and processed to obtain cytospins and supernatant. The statistical power to detect a 20% difference in sputum parameters was > 90%. Results are expressed as median and interquartile range [IQR]. Induced sputum had a higher proportion of viable cells (77.0 [19.0] versus 47.0 [38.0]%, p < 0.001), less squamous cell contamination (1.0 [1.2] versus 1.8 [34.0]%, p < 0.001) and better quality cytospins (score of 8.0 [4.0] versus 4.0 [2.0], p < 0.001). It also had lower fluid-phase levels of eosinophil cationic protein (ECP) (1,358 [1,102] versus 1,574 [2,479] microg/L) and fibrinogen (1,560.0 [3,130.0] versus 4,350.0 [5,970.0] ng/ml) but only the latter was significantly different (p = 0.02). Induced sputum was similar to spontaneous sputum in weight (200.0 [219.0] versus 270.0 [227.0] mg), total cell count (3.3 [4.1] versus 3.5 [4.5] x 10(6)/ml), proportion of nonsquamous cells, and levels of tryptase. The agreement between induced and spontaneous measurements was good, but fluid-phase levels were affected by the low viability of some spontaneous samples. We conclude that for the indices measured in asthmatic subjects, induced sputum separated from saliva is similar to lower respiratory secretions expectorated spontaneously and has the advantage of better cell viability.
"This article explores the impact of the Coalition Government's proposals to limit recently-arrived migrants' access to social welfare benefits [in Australia]. It concludes that while the short-term consequences for these migrants will be severe, the proposals do not address the more significant long-term welfare costs of family migration."
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