bluuebunny/crossref_metadata_2025_split huggingface dataset:
The management of breech pregnancies in Australia and New Zealand
Authors: Phipps Hala , Roberts Christine L. , Nassar Natasha , Raynes‐Greenow Camille H. , Peat Brian , Hutton Eileen K. 
Published: July 2003

AbstractAim: To assess current obstetric practice in the management of singleton breech pregnancies in Australia and New Zealand.Methodology: Survey mailed to all members and fellows of the Royal Australian and New Zealand College of Obstetrics and Gynaecology.Results : Of 1284 surveyed, 956 (74%) responded of whom 696 (73%) were practicing obstetrics. Prior to the Term Breech Trial (TBT), 72% of obstetricians reported that they routinely offered vaginal breech birth for uncomplicated singleton breech pregnancies. After the TBT publication this rate declined to 20%. External cephalic version (ECV) was usually recommended by 67% of obstetricians and only 53% use tocolytics. Common practices for which safety has yet to be demonstrated included 28% of obstetricians carrying out ECV outside hospitals and 42% carrying out ECV before 37 weeks’ gestation.Conclusions : While the majority of obstetricians recommend ECV and/or planned Caesarean section for breech presentation, barriers to the promotion of ECV and the use of tocolysis for ECV need to be identified if the rates of this effective manoeuvre are to be increased.
Use of umbilical artery Doppler velocimetry in the monitoring of pregnancy in women with pre‐existing diabetes
Authors: Wong Shell Fean , Chan Fung Yee , Cincotta Robert B , McIntyre David H , Stone Murray 
Published: July 2003

AbstractBackground:  The usefulness of umbilical artery Doppler velocimetry for the monitoring of diabetic pregnancies is controversial. The aim of the present study was to assess whether umbilical artery Doppler velocity waveform analysis can predict adverse perinatal outcomes for pregnancies complicated by pre‐existing diabetes mellitus.Methods:  All diabetic pregnancies (type 1 and 2) delivered at Mater Mothers’ Hospital, Queensland, between 1 January 1995 and 31 December 1999 were included. All pregnant diabetic women were monitored with umbilical artery Doppler velocimetry at 28, 32, 36, and 38 weeks’ gestation. Adverse perinatal outcome was defined as pregnancies with one or more of the following: small‐for‐gestational age, Caesarean section for non‐reassuring cardiotocography, fetal acidaemia at delivery, 1‐min Apgar of 3 or less, 5‐min Apgar of less than 7, hypoxic ischaemic encephalopathy or perinatal death. Abnormal umbilical artery Doppler velocimetry was defined as a pulsatility index of 95th centile or higher for gestation.Results:  One hundred and four pregnancies in women with pre‐existing diabetes had umbilical arterial Doppler studies carried out during the study period. Twenty‐three pregnancies (22.1%) had an elevated pulsatility index. If the scans were carried out within 2 weeks of delivery, 71% of pregnancies with abnormal umbilical Doppler had adverse outcomes (P < 0.01; likelihood ratio, 4.2). However, the sensitivity was 35%; specificity was 94%; positive predictive value was 80%; and negative predictive value was 68%. Only 30% of women with adverse perinatal outcomes had abnormal umbilical arterial Doppler flow.Conclusion:  Umbilical artery Doppler velocimetry is not a good predictor of adverse perinatal outcomes in diabetic pregnancies.
Signalling to glucose transport in skeletal muscle during exercise
Authors: Richter E. A. , Nielsen J. N. , Jørgensen S. B. , Frøsig C. , Wojtaszewski J. F. P. 
Published: July 2003

AbstractExercise‐induced glucose uptake in skeletal muscle is mediated by an insulin‐independent mechanism. Although the signalling events that increase glucose transport in response to muscle contraction are not fully elucidated, the aim of the present review is to briefly present the current understanding of the molecular signalling mechanisms involved. Glucose uptake may be regulated by Ca++‐sensitive contraction‐related mechanisms possibly involving protein kinase C, and by mechanisms that reflect the metabolic status of the muscle and may involve the AMP‐activated protein kinase. Furthermore the p38 mitogen activated protein kinase may be involved. Still, the picture is incomplete and a substantial part of the exercise/contraction‐induced signalling mechanism to glucose transport remains unknown.
Musculoskeletal manifestations in patients with thyroid disease
Authors: Cakir Mehtap , Samanci Nehir , Balci Nilufer , Balci Mustafa Kemal 
Published: July 2003

SummaryobjectiveThyroid dysfunction may cause musculoskeletal symptoms. We have evaluated the prevalence of adhesive capsulitis, Dupuytren's contracture, trigger finger, limited joint mobility and carpal tunnel syndrome in a series of patients with various thyroid diseases and differing levels of function.design and patientsPatients with euthyroid (diffuse and/or nodular) goitre, Hashimoto's thyroiditis, Graves’ disease, toxic nodular goitre, toxic diffuse goitre and patients with goitre who had partial thyroidectomy were included in the study (n = 137). Neurological and musculoskeletal examinations were performed after a standardized symptom questionnaire. The prevalence of musculoskeletal problems was analysed with respect to thyroid function and thyroid autoantibody status.measurementsSerum concentrations of free T3, free T4, TSH and thyroglobulin and thyroperoxidase antibodies were determined. Serum levels of creatine kinase, lactate dehydrogenase, calcium and phosphate along with erythrocyte sedimentation rate were measured to exclude other causes of musculoskeletal complaints.resultsWhen the study group (n = 137) was divided according to thyroid status, 30·6% (n = 42) were thyrotoxic, 16·8% (n = 23) had subclinical thyrotoxicosis, 28·5% (n = 39) were euthyroid, 7·3% (n = 10) had subclinical hypothyroidism and 16·8% (n = 23) were hypothyroid. Overall, adhesive capsulitis was found in 10·9% (n = 15), Dupuytren's contracture in 8·8% (n = 12), limited joint mobility in 4·4% (n = 6), trigger finger in 2·9% (n = 4) and carpal tunnel syndrome in 9·5% (n = 13) of the patients. The prevalence of adhesive capsulitis was highest in patients with subclinical thyrotoxicosis (17·4%); Dupuytren's contracture, limited joint mobility and carpal tunnel syndrome were commonest in hypothyroid patients (21·7%, 8·7% and 30·4%, respectively). Trigger finger occurred in 10% of patients with subclinical hypothyroidism. When these prevalences were analysed with respect to thyroid status, carpal tunnel syndrome was significantly more prevalent in the hypothyroid group (P = 0·004). When thyroperoxidase antibody‐positive and ‐negative patients were compared, adhesive capsulitis negatively (P = 0·03,r =−0·18) and trigger finger positively correlated with (P = 0·03,r = 0·21) thyroperoxidase antibody existence.conclusionsThese results demonstrate that musculoskeletal disorders often accompany thyroid dysfunction. In addition to the well‐known observation that these disorders are common in patients with hypothyroidism, they are also observed in patients with thyrotoxicosis. Patients with thyroid dysfunction should be questioned for musculoskeletal complaints and referred to a specialist if necessary.
The effect of pegvisomant‐induced serum IGF‐I normalization on serum leptin levels in patients with acromegaly
Authors: Parkinson C. , Whatmore A. J. , Yates A. P. , Drake W. M. , Brabant G. , Clayton P. E. , Trainer P. J. 
Published: July 2003

Summarybackground In humans, serum leptin correlates positively with fat mass. GH is lipolytic and patients with active acromegaly have lowered serum leptin compared to age, sex and body mass index (BMI)‐matched controls, but a direct influence of GH on serum leptin remains unclear. In patients with acromegaly, total leptin increases following successful pituitary surgery and during somatostatin (SMS) analogue therapy (despite no change in BMI) but whether this represents changes in soluble leptin receptor, bound or free leptin is unclear. Pegvisomant, a GH receptor antagonist capable of normalizing serum IGF‐I in over 97% of patients, represents a novel treatment strategy in acromegaly and its effect on leptin has not previously been reported.patients Sixteen patients (nine male (M), seven female (F), median age 52 years, range 27–78 years) with active acromegaly (serum IGF‐I at least 30% above the upper limit of an age‐related reference range) were studied. Serum IGF‐I was normalized in all subjects with pegvisomant [mean duration 7 months (range 3–11 months), median dose 20 mg/day (range 10–40 mg/day)]. A single batch measurement of leptin, bound leptin (BL), soluble leptin receptor (SLR), insulin and glucose were performed on samples from baseline and first occurrence of serum IGF‐I normalization.results As in normal subjects, females with acromegaly had higher baseline serum leptin [median M = 6·1 (range 1·6–58·7), F = 25·9 (range 3·19–54·1) ng/ml; P = 0·04], which correlated positively with BMI (R = 0·78, P = 0·0004). Forward step‐wise regression analysis demonstrated that BMI and gender accounted for 90% of the variance in mean serum log10 leptin. Pegvisomant‐induced serum IGF‐I normalization was associated with a rise in serum leptin [8·9 (range 1·6–58·3) to 12·7 (range 2·3–90·8) ng/ml, P < 0·0001]. Although the absolute increase was not significantly different, mean percentage increase was greater in men (M = 66·6 ± 51%, F = 11·8 ± 16%, P = 0·017) despite similar serum IGF‐I and BMI in male and female subjects at baseline. No change in BL or SLR accompanied serum IGF‐I normalization [0·27 (range 0·15–1·26) to 0·27 (range 0·14–1·2) nmol/l, P = 0·27 and 3·2 (range 1·2–6·8) to 2·7 (range 1–7·4) nmol/l, P = 0·5, respectively]. After normalization of serum IGF‐I, a correlation between BMI and leptin remained (R = 0·86, P < 0·0001) and together BMI and gender accounted for 87% of the variance in mean log10 serum leptin (P = 0·0002).conclusion Pegvisomant‐induced serum IGF‐I normalization in patients with active acromegaly is associated with a significant increase in total, and by implication, free leptin.
Mutational analyses of RB and BRCA2 as candidate tumour suppressor genes in parathyroid carcinoma
Authors: Shattuck Trisha M. , Kim Teresa S. , Costa Jessica , Yandell David W. , Imanishi Yasuo , Palanisamy Nallasivam , Gaz Randall D. , Shoback Dolores , Clark Orlo H. , Monchik John M. , Wierman Margaret E. , Hollenberg Anthony , Tojo Katsuyoshi , Chaganti R. S. K. , Arnold Andrew 
Published: July 2003

Summaryobjective Strong evidence indicates that at least one key tumour suppressor gene important for the development of malignant parathyroid tumours is located on chromosome 13, but the critical target gene remains unknown. Importantly, the region of acquired DNA loss includes two established tumour suppressor genes, the retinoblastoma gene, RB (RB1) and BRCA2. Resolution of whether RB or BRCA2 is the critical 13q tumour suppressor gene in parathyroid cancer requires analysis of these genes’ sequences for intragenic inactivating mutations. Therefore, RB and BRCA2 were analysed in a group of parathyroid carcinomas in which mutations of these genes should be most readily detectable.patients and design Six parathyroid carcinomas from four patients which showed loss of heterozygosity (LOH) at the RB locus and/or 13q loss by comparative genomic hybridazation (CGH) were selected from a CGH/LOH‐screened panel of 16 carcinoma specimens from 10 patients. These tumours were examined for mutations by direct sequencing of the complete 27‐exon coding region, intron–exon boundaries and promoter of RB. The 26 coding exons and intron–exon boundaries of BRCA2 were also directly sequenced in seven parathyroid carcinomas with loss in the BRCA2 region.results No microdeletions, insertions, or point mutations were detected in either RB or BRCA2 in any of the carcinomas.conclusion The absence of tumour‐specific somatic mutations in RB and BRCA2 suggests that they are unlikely to act as classic tumour suppressor genes in the pathogenesis of parathyroid carcinomas. While decreased expression of these genes might contribute to parathyroid carcinomatosis in a secondary fashion and 13q loss warrants further study as a diagnostic marker for parathyroid carcinoma, the putative 13q tumour suppressor awaits identification.
The effect of body weight and weight loss on thyroid volume and function in obese women
Authors: Sari Ramazan , Balci Mustafa Kemal , Altunbas Hasan , Karayalcin Umit 
Published: July 2003

Summaryobjective Thyroid volume and thyroid function may vary in obese and nonobese women. It is not known whether weight loss could affect thyroid volume and function in obese subjects.patients and methods The study population consisted of 98 premenopausal euthyroid obese [body mass index (BMI) = 30 kg/m2] women (mean age 40·5 ± 11·4 years) and 31 nonobese (BMI < 25 kg/m2) women (mean age 38·6 ± 12·9 years). Weight, height, BMI, waist circumference, body fat percentage and fat weight of all subjects were measured. Thyroid function and thyroid ultrasonography were performed at baseline and after 6 months of obesity treatment. Subgroup analysis was done according to weight loss.results Thyroid volume (P = 0·021) and TSH concentration (P = 0·047) were higher; free T3 (P < 0·001) and free T4 concentrations (P = 0·045) were lower in obese women; however, all were still in the normal range. There was a positive correlation between thyroid volume and body weight (r = 0·319, P = 0·002), BMI (r = 0·504, P < 0·001), body fat percentage (r = 0·375, P = 0·001), body fat weight (r = 0·309, P = 0·01) and waist circumference (r = 0·386, P = 0·004). There was a positive correlation between TSH concentration and body weight (r = 0·227, P = 0·042) and body fat weight (r = 0·268, P = 0·038). After 6 months of obesity treatment, thyroid volume (P = 0·008) and TSH concentration (P = 0·006) decreased only in obese women who lost > 10% body weight. There was a positive correlation between the changes of thyroid volume and the change of body weight (r = 0·341, P = 0·009) and the change of body fat weight (r = 0·406, P = 0·013).conclusions Our study suggests that thyroid volume and function may vary in obese women in association with body weight and fat mass; > 10% weight loss may affect thyroid volume and function, which however, is clinically insignificant.
ACE DD genotype: an independent predisposition factor to venous thromboembolism
Authors: Fatini C. , Gensini F. , Sticchi E. , Battaglini B. , Prisco D. , Fedi S. , Brunelli T. , Marcucci R. , Conti A. A. , Gensini G. F. , Abbate R. 
Published: July 2003

AbstractBackground The renin angiotensin system affects haemostasis through different mechanisms; data on the possible role of angiotensin‐converting enzyme I/D polymorphism in the pathogenesis of deep venous thrombosis are conflicting, and no information is available regarding the A1166C polymorphism of the angiotensin type 1 receptor gene. In order to investigate this issue, angiotensin‐converting enzyme and AT1R polymorphisms were genotyped in 336 consecutive venous thromboembolism patients and 378 controls.Materials and methods Haemostasis‐related risk factors have been evaluated by routine tests. Factor V Leiden, Factor II (G20210A), angiotensin‐converting enzyme (I/D), and angiotensin type 1 receptor (A1166C) polymorphisms have been identified by molecular analysis.Results We documented a significant association between angiotensin‐converting enzyme DD genotype and venous thromboembolism (OR = 2·19 95%CI 1·51–3·17 adjusted for acquired and haemostasis‐related risk factors, P < 0·0001); in patients with haemostasis‐related risk factors, angiotensin‐converting enzyme DD genotype modified the risk of venous thromboembolism in hyperhomocysteinaemic and Factor V Leiden patients and was associated with the risk of recurrent venous thromboembolism (OR = 1·83 95%CI 1·06–3·17 P = 0·03). In patients without haemostasis‐related risk factors the angiotensin‐converting enzyme DD genotype was still an independent predictor of venous thromboembolism (OR = 3·29 95%CI 2·17–4·98 adjusted for acquired risk factors, P < 0·0001). No significant association between the angiotensin type 1 receptor CC genotype and venous thromboembolism was found.Conclusions This study shows that angiotensin‐converting enzyme DD genotype represents a susceptibility marker of thrombosis in subjects apparently without predisposing factors and traditional thrombophilic alterations, and increases the risk of venous thromboembolism in subjects in whom a thrombogenic condition occurs. Moreover, angiotensin‐converting enzyme DD genotype may be considered a new predisposing factor to venous thromboembolism recurrence.
Metalloproteinases 2 and 9 are increased in plasma of patients with heart failure
Authors: Altieri P. , Brunelli C. , Garibaldi S. , Nicolino A. , Ubaldi S. , Spallarossa P. , Olivotti L. , Rossettin P. , Barsotti A. , Ghigliotti G. 
Published: July 2003

AbstractBackground Progression of heart failure is associated with interstitial changes in the heart and in areas distant from the heart. Enhanced expression of metalloproteinases 2 and 9 and of metalloproteinases tissue inhibitors 1 and 2 have been found in ventricular tissue of patients with heart failure. Our aim was to determine whether increased activity of metalloproteinase‐2, metalloproteinase‐9 and of metalloproteinases tissue inhibitor‐1 and metalloproteinases tissue inhibitor‐2 were also present in plasma of patients with heart failure.Design Levels of metalloproteinase‐2, metalloproteinase‐9 and of metalloproteinase tissue inhibitor‐1 and metalloproteinases tissue inhibitor‐2 were measured in venous blood of 51 patients with heart failure, and were compared with levels of 52 control subjects. Samples collected from patients and control subjects were assayed for gelatinolytic activity (zymography) and for protein levels.Results Compared with the control subjects, the patients with heart failure had a significant increase in activity levels (mean ± SE, ng mL−1) of prometalloproteinase‐9 (95·1 ± 11·2 and 38·9 ± 4·5*), activ. metalloproteinase‐9 (18·4 ± 2·5 and 10·9 ± 1·3*), and of prometalloproteinase‐2 (571·4 ± 26·1 and 456·8 ± 21·1*) (respectively: patients and control sub jects; *P < 0·05). Metalloproteinases tissue inhibitor‐1, but not metalloproteinases tissue inhibitor‐2 protein values were higher in the patients. Among the patients, clinical status and New York Heart Association (NYHA) class did not correlate with the metalloproteinase concentrations. Positive correlations with left ventricular volumes, and negative correlations with lipid values were obtained for prometalloproteinase‐2; positive correlations with total number of white cells and neutrophils were obtained for prometalloproteinase‐9; and positive correlations with lactate dehydrogenase, serum fibrinogen, aspartate transaminases were found for activ. metalloproteinase‐9.Conclusions Regardless of the clinical phase of heart failure, elevated levels of activity and of circulating metalloproteinase protein levels suggest the presence of persistent extracellular remodeling in patients with heart failure.
Immunoglobulin light chains modulate polymorphonuclear leucocyte apoptosis
Authors: Cohen G. , Rudnicki M. , Deicher R. , Hörl W. H. 
Published: July 2003

AbstractBackground Apoptosis of polymorphonuclear leucocytes (PMNLs) is important for the resolution of inflammation. Recently, we demonstrated that glucose‐modified proteins increase PMNL apoptosis. No protein factors in sera of uraemic patients attenuating PMNL apoptosis have been identified to date.Materials and methods We tested the influence of commercially available monoclonal immunoglobulin light chains (IgLCs) from multiple myeloma patients and polyclonal IgLCs isolated from haemodialysis patients, previously shown to modulate PMNL functions and to contribute to their prestimulation, on PMNL apoptosis. We detected morphological changes, DNA strand breaks and the loss of DNA content.Results All three apoptosis assays showed that κ and λ type IgLCs increase the percentage of viable PMNLs by inhibiting apoptosis in a concentration‐dependent manner. The effect of IgLCs was abolished by specific antibodies. Addition of genistein abolished the reduction of PMNL apoptosis by IgLCs, suggesting that IgLCs exert their effect via tyrosine phosphorylation. Furthermore, we showed that the inhibition of caspase‐3 activity is involved in the decrease of PMNL apoptosis.Conclusion In concentrations present in sera of uraemic patients IgLCs could interfere with the normal resolution of inflammation and thereby contribute to the chronic inflammatory state found in end‐stage renal disease patients.
Diagnosis of diabetic autonomic neuropathy: a multivariate approach
Authors: Diem P. , Laederach‐Hofmann K. , Navarro X. , Mueller B. , Kennedy W. R. , Robertson R. P. 
Published: July 2003

AbstractAim/hypothesis In the diagnosis of diabetic autonomic neuropathy (DAN) various autonomic tests are used. We took a novel statistical approach to find a combination of autonomic tests that best separates normal controls from patients with DAN.Methods Twenty‐four patients with Type‐1 diabetes mellitus considered as having mild to moderate DAN as well as 10 normal, nondiabetic control subjects were analysed, searching for a test or a combination of tests that would optimally discriminate Type‐1 diabetes mellitus from controls. Variations of heart rate during deep breathing (ΔR6) and during a Valsalva manoeuvre (VR), the number of reactive sweat glands on the foot (testing sympathetic sudomotor function), and the response of human pancreatic polypeptide to hypoglycaemia [ln(ΔhPP + 1)] were evaluated.Results Respective values for respective sensitivity and specificity values were: ΔR6, 96 and 70%; VR, 96 and 60%; sweat gland function, 71 and 90%; and ln(ΔhPP + 1), 71 and 90%. In a multivariate analysis approach a single discriminant function separating patients with Type‐1 diabetes mellitus from nondiabetic controls was generated {Logit P = 288·5 –[14·7 ΔR6]–[26·6 ln(ΔhPP + 1)]}. This function allowed complete separation of patients with Type‐1 diabetes mellitus from normal controls.Conclusion/interpretation We conclude that the combined determination of ΔR6 and of ln (ΔhPP + 1) optimally separates subjects with parasympathetic impairment from normal subjects. In addition, this combination of tests may serve as a sensitive method for the assessment of DAN.
Do temporal arteritis lesions contain bacterial DNA?
Authors: Renko J. , Kalela A. , Karhunen P. J. , Helin H. , Sillanaukee P. , Nikkari S. , Nikkari S. T. 
Published: July 2003

AbstractBackground Temporal arteritis is a primary vascular inflammatory disease. The aetiology of temporal arteritis is unknown, but the influence of environmental factors such as infections has been suggested.Materials and methods We used broad‐range PCR, targeting conserved regions of the gene encoding for ribosomal RNA, to detect bacterial DNA in 27 temporal artery biopsies. Five uninvolved temporal arteries were also included. A lung sample of confirmed bacterial pneumonia served as a positive control. Inflammation was examined by histochemistry and light microscopy.Results The sensitivity of the broad‐range PCR assay was 5·0 fg of DNA. Bacterial DNA sequences were neither detected in 27 temporal arteritis specimens nor in the normal temporal artery samples. However, bacterial DNA was successfully amplified from the lung sample of a subject with pneumonia. In addition, human DNA was amplified by primers for human β‐actin from all clinical specimens, suggesting lack of significant inhibitors of the molecular amplification reaction. Histochemistry showed signs of strong inflammation in the arteritis samples.Conclusions The lack of detectable amounts of bacterial DNA suggests that viable bacteria do not have a role in chronic stages of temporal arteritis. However, these findings do not rule out the possibility of bacterial degradation products as stimulants of chronic inflammation, or of viable microbes as triggering factors of acute temporal arteritis.