bluuebunny/crossref_metadata_2025_split huggingface dataset:
Risk factors for hypertension during pregnancy in South Australia
Authors: Jacobs Daniëlle J. , Vreeburg Sophie A. , Dekker Gus A. , Heard Adrian R. , Priest Kevin R. , Chan Annabelle 
Published: November 2003

AbstractObjective: To identify risk factors for hypertension in pregnancy among South Australian women.Design: A population‐based retrospective analysis using the South Australian perinatal data collection for 1998–2001.Methods: Three groups of women with hypertension (pre‐existing hypertension, pregnancy hypertension, and superimposed pre‐eclampsia) were compared with normotensive women using unconditional logistic regression analysis on 70 386 singleton births to identify sociodemographic and clinical risk factors for hypertension in pregnancy.Results:  Nulliparity, Aboriginal race and Caucasian race (compared with Asian) and pre‐existing and gestational diabetes were demonstrated to be risk factors for all hypertensive disorders, as was increasing maternal age for pre‐existing hypertension and superimposed pre‐eclampsia. Risk was increased for pregnancy hypertension and superimposed pre‐eclampsia among women who gave their occupation as ‘home duties’ and also for superimposed pre‐eclampsia among unemployed women. Women with hypertension were more likely to give birth in teaching hospitals. Urinary tract infections were not found to be a risk factor for any type of hypertension. Smoking during pregnancy was protective for all types of hypertension.Conclusions: The present study used a statewide population perinatal database and has confirmed that Aboriginal race, Caucasians, nulliparity, and pre‐existing and gestational diabetes are independent risk factors for all types of hypertension in pregnancy. Increasing maternal age increased the risk for pre‐existing hypertension and superimposed pre‐eclampsia. There appeared to be appropriate referral of women with hypertensive disorders to teaching hospitals. A new finding is the increased risk among unemployed women and women engaged in home duties.
Simulating evolution of glyphosate resistance in Lolium rigidum II: past, present and future glyphosate use in Australian cropping
Authors: Neve P , Diggle A J , Smith F P , Powles S B 
Published: November 2003

SummaryGlyphosate is a key component of weed control strategies in Australia and worldwide. Despite widespread and frequent use, evolved resistance to glyphosate is rare. A herbicide resistance model, parameterized for Lolium rigidum has been used to perform a number of simulations to compare predicted rates of evolution of glyphosate resistance under past, present and projected future use strategies. In a 30‐year wheat, lupin, wheat, oilseed rape crop rotation with minimum tillage (100% shallow depth soil disturbance at sowing) and annual use of glyphosate pre‐sowing, L. rigidum control was sustainable with no predicted glyphosate resistance. When the crop establishment system was changed to annual no‐tillage (15% soil disturbance at sowing), glyphosate resistance was predicted in 90% of populations, with resistance becoming apparent after between 10 and 18 years when sowing was delayed. Resistance was predicted in 20% of populations after 25–30 years with early sowing. Risks of glyphosate resistance could be reduced by rotating between no‐tillage and minimum‐tillage establishment systems, or by rotating between glyphosate and paraquat for pre‐sowing weed control. The double knockdown strategy (sequential full rate applications of glyphosate and paraquat) reduced risks of glyphosate and paraquat resistance to <2%. Introduction of glyphosate‐resistant oilseed rape significantly increased predicted risks of glyphosate resistance in no‐tillage systems even when the double knockdown was practised. These increased risks could be offset by high crop sowing rates and weed seed collection at harvest. When no selective herbicides were available in wheat crops, the introduction of glyphosate‐resistant oilseed rape necessitated a return to a minimum‐tillage crop establishment system.
Simulating evolution of glyphosate resistance in Lolium rigidum I: population biology of a rare resistance trait
Authors: Neve P , Diggle A J , Smith F P , Powles S B 
Published: November 2003

SummaryDespite frequent use for the past 25 years, resistance to glyphosate has evolved in few weed biotypes. The propensity for evolution of resistance is not the same for all herbicides, and glyphosate has a relatively low resistance risk. The reasons for these differences are not entirely understood. A previously published two‐herbicide resistance model has been modified to explore biological and management factors that account for observed rates of evolution of glyphosate resistance. Resistance to a post‐emergence herbicide was predicted to evolve more rapidly than it did to glyphosate, even when both were applied every year and had the same control efficacy. Glyphosate is applied earlier in the growing season when fewer weeds have emerged and hence exerts less selection pressure on populations. The evolution of glyphosate resistance was predicted to arise more rapidly when glyphosate applications were later in the growing season. In simulations that assumed resistance to the post‐emergence herbicide did not evolve, the evolution of glyphosate resistance was less rapid, because post‐emergence herbicides were effectively controlling rare glyphosate‐resistant individuals. On their own, these management‐related factors could not entirely account for rates of evolution of resistance to glyphosate observed in the field. In subsequent analyses, population genetic parameter values (initial allele frequency, dominance and fitness) were selected on the basis of empirical data from a glyphosate‐resistant Lolium rigidum population. Predicted rates of evolution of resistance were similar to those observed in the field. Together, the timing of glyphosate applications, the rarity of glyphosate‐resistant mutants, the incomplete dominance of glyphosate‐resistant alleles and pleiotropic fitness costs associated with glyphosate resistance, all contribute to its relatively slow evolution in the field.
Progression of destructive periodontal diseases in three urban minority populations: role of clinical and demographic factors
Authors: Craig Ronald G. , Yip Julie K. , Mijares Dindo Q. , LeGeros Racquel Z. , Socransky Sigmund S. , Haffajee Anne D. 
Published: November 2003

AbstractBackground, aims: Differences in prevalence, severity and risk factors for destructive periodontal diseases have been reported for ethnic/racial groups. However, it is not certain whether this disparity is due to ethnicity/race or factors associated with ethnicity/race. Therefore, the present study addressed whether the rates of disease progression and clinical and demographic factors associated with disease progression varied among three ethnic/racial groups.Methods: The study population consisted of 53 Asian‐, 69 African‐ and 62 Hispanic‐Americans. Clinical measurements included probing depth, attachment level, gingival erythema, bleeding upon probing, suppuration and plaque. Disease progression was defined as a >2 mm loss of attachment 2 months post baseline. The demographic variables examined included occupational status, report of a private dentist, years resident in the United States and smoking history.Results: The rate of attachment loss for the entire population was 0.04 mm or 0.24 mm/year. No significant differences were found among the three ethnic/racial groups. Variables associated with subsequent attachment loss for the entire population were age, male gender, mean whole‐mouth plaque, erythema, bleeding upon probing, suppuration, attachment loss and probing depth, and belonging to the “unskilled” occupational group. No differences in risk profiles were found among the 3 ethnic/racial groups. Using stepwise logistic regression analysis, a model was developed to relate the clinical and demographic variables examined with subsequent attachment loss. The model indicated that prior attachment loss, gingival erythema, suppuration, being a current smoker and belonging to the “unskilled” occupational group conferred high risk of >1 site of attachment loss of >2 mm.Conclusions: The results of this study suggest that variables associated with ethnicity/race, such as occupational status, are largely responsible for the observed disparity in destructive periodontal disease progression in these populations.
Demonstration of Feline Foamy Virus in Experimentally Infected Cats by Immunohistochemistry
Authors: Weikel J. , Löchelt M. , Truyen U. 
Published: November 2003

SummaryFoamy viruses (FV) are complex retroviruses which are commonly isolated from cats, cattle and non‐human primates. The infection is persistent and infected animals have a sustained antibody response. The role of FV in diseases remains unclear, in cats, a possible association with uncharacterized renal symptoms remains to be confirmed. To demonstrate feline FV (FFV) in tissues of experimentally infected cats three polyclonal monospecific antisera from rabbits against three different viral proteins, the structural Gag and the non‐structural Bel 1 and Bet proteins were tested for their applicability in immunohistochemistry with paraffin sections. Only the Bet antiserum allowed detection of FFV‐specific proteins, the antibodies against Gag and Bel 1 did not work even after pre‐treatment of the slides with proteinase K or cooking in a pressure cooking pot. The Bet‐reactive antibodies were detected using a commercial streptavidin kit and revealed Bet in the cytoplasm of cells from different lymphoid tissues like lymphnodes, tonsils, thymus and spleen. The method described opens new ways to explore the in vivo replication and tissue specificity of FFV and its possible role in disease.
Brief exposures of resting fibroblasts to okadaic acid stimulate DNA synthesis
Authors: Setkov N. A. , Epifanova O. I. 
Published: November 2003

AbstractTo study further the factors providing for cellular quiescence, we used okadaic acid (OA) at concentrations (0.1, 1, 10 or 100 nM) inhibiting type 1 and/or type 2A protein phosphatases in mammalian cell cultures. Brief (2 h) exposure of resting (0.2% serum for 72 h) NIH 3T3 mouse fibroblasts to OA with subsequent incubation of cells in a medium with 0.2% serum, stimulated DNA synthesis at all concentrations studied. Maximal stimulation was observed following pre‐incubation of resting cells with 10 nM OA. Treatment of cycling cells (10% serum) with OA (2 h pulses at 12 h intervals for 72 h) prevented their exit to the resting state on transfer to a medium with 0.2% serum. Brief exposures of resting cells to OA did not affect the rate of protein synthesis. OA pulses in the late pre‐replicative period had no effect on the entry of serum‐stimulated cells into the S phase.Cell fusion experiments with resting (serum‐deprived) and proliferating (serum‐stimulated) NIH 3T3 cells, using radioautography with a double‐labelling technique, revealed that pre‐incubation of resting cells with OA for 2 h before and after fusion abrogates their ability to suppress the onset of DNA synthesis in the nuclei of proliferating cells in heterodikaryons. The results indicate that protein phosphatases of type 1 and/or 2A may be involved in the growth‐arrest machinery that provides for cellular quiescence.
Serum deprivation induces SV40 early promoter activity
Authors: Tzen C.‐Y. , Scott R. E. , Robinson F. D. 
Published: November 2003

AbstractProliferation and the expression of proliferation‐associated genes are modulated by changing the serum concentration in the media of cultured cells. To determine if activity of the SV40 early promoter is modulated by serum, we examined the expression of SV40 early promoter driven marker genes in murine BALB/c 3T3T cells following serum deprivation or serum stimulation. SV40‐promoter‐regulated β‐galactosidase and chloramphenicol acetyl transferase genes were studied following either transient or stable transfection. The results show that serum deprivation of growing cells induces SV40 promoter activity while serum stimulation of quiescent G0 cells suppresses it. Kinetic analyses show a significant induction of the SV40 promoter activity during the first 2 days of serum deprivation which is maintained at a high level for 15 days. The induction of reporter gene expression by serum deprivation was selective for the SV40 early promoter because such an effect was not observed using the Rous sarcoma viral promoter. Nuclear run‐off assays further show that the transcription controlled by the SV40 early promoter is ∼ twofold greater in cells rendered quiescent by serum deprivation for 72 h than in growing cells cultured in medium containing serum. These results suggest that one reason SV40 T transformed cells commonly fail to undergo quiescence following serum deprivation is that the SV40 promoter is induced.
Recombinant hGH replacement therapy and the hypothalamus–pituitary–thyroid axis in children with GH deficiency: when should we be concerned about the occurrence of central hypothyroidism?
Authors: Giavoli Claudia , Porretti Silvia , Ferrante Emanuele , Cappiello Vincenzo , Ronchi Cristina L. , Travaglini Pietro , Epaminonda Paolo , Arosio Maura , Beck‐Peccoz Paolo 
Published: November 2003

Summaryobjective  Recombinant hGH treatment may alter thyroid hormone metabolism and we have recently reported that 50% of patients with GH deficiency (GHD) due to organic lesions, previously not treated with thyroxine, developed hypothyroidism during treatment with recombinant human GH (rhGH). These results prompted us to evaluate the impact of rhGH treatment on thyroid function in children with GHD.design  Open study of GH treatment up to 12 months. Investigations were performed at baseline, and after 6 and 12 months of GH therapy.measurement and study subjects  Serum TSH, FT4, FT3, AbTg and AbTPO, IGF‐I, height and weight, were evaluated in 20 euthyroid children (group A) with idiopathic isolated GHD and in six children (group B) with multiple pituitary hormone deficiencies (MPHD) due to organic lesions. Among the latter, four already had central hypothyroidism and were on adequate LT4 replacement therapy, while two were euthyroid at the beginning of the study.results  Serum IGF‐I levels normalized in all patients. In both groups, a significant reduction in FT4 levels (P < 0·01) occurred during rhGH therapy. No patient in group A had FT4 values into the hypothyroid range, while in four of six patients in group B, fell FT4 levels into the hypothyroid range during rhGH. In particular, the two euthyroid children developed central hypothyroidism during rhGH treatment, and their height velocities did not normalize until the achievement of euthyroidism through appropriate LT4 substitution. No variation in serum FT3 and TSH levels was recorded in either groups.conclusion  Contrary to that observed in patients with MPHD, rhGH replacement therapy does not induce central hypothyroidism in children with idiopathic isolated GHD, further supporting the view that in children with MPHD, as in adults, GHD masks the presence of central hypothyroidism. Slow growth (in spite of adequate rhGH substitution and normal IGF‐I levels) is an important clinical marker of central hypothyroidism, therefore a strict monitoring of thyroid function is mandatory in treated children with MPHD.
Metabolic, inflammatory and haemostatic effects of a low‐dose continuous combined HRT in women with type 2 diabetes: potentially safer with respect to vascular risk?
Authors: McKenzie Joyce , Jaap Alan J. , Gallacher Stephen , Kelly Anne , Crawford Lynne , Greer Ian A. , Rumley Ann , Petrie John R. , Lowe Gordon D. , Paterson Kenneth , Sattar Naveed 
Published: November 2003

Summarybackground  Conventional hormone replacement therapy (HRT) containing conjugated equine oestrogen (CEE) and medroxyprogesterone acetate (MPA) increases triglyceride, C‐reactive protein (CRP) and coagulation Factor VII concentrations, potentially explaining their increased coronary heart disease (CHD) and stroke risk.objective  To assess the metabolic effects of a continuous combined HRT containing 1 mg oestradiol and 0·5 mg norethisterone or matching placebo.design  Double‐blind, randomized placebo‐controlled trial.patients  Fifty women with type 2 diabetes.measurements  Classical and novel risk factors for vascular disease.results  Triglyceride concentration was not altered (P = 0·31, change in active arm relative to placebo) and low‐density lipoprotein (LDL) cholesterol concentration declined 13% (P = 0·018). IL‐6 concentration (mean difference −1·42 pg/ml, 95% CI: −2·55 to –0·29 IU/dl, P = 0·015), Factor VII (−32 IU/dl, −43 to −21 IU/l, P < 0·001) and tissue plasminogen activator antigen (by 13%, P = 0·005) concentrations fell, but CRP was not significantly altered (P = 0·62). Fasting glucose (P = 0·026) also declined significantly, but there are no significant effects on HBA1c, Factor IX or APC resistance.conclusions  HRT containing 1 mg oestradiol and 0·5 mg norethisterone may avoid the adverse metabolic effects potentially implicated in the elevated CHD and stroke risk induced by conventional higher dose HRT. This type of preparation may therefore be more suitable than conventional HRT for women at elevated CHD risk such as those with type 2 diabetes. Large randomized controlled trials of such low dose preparations, powered for cardiovascular end points, are now needed.
Serum leptin levels in patients with premenstrual syndrome treated with GnRH analogues alone and in association with tibolone
Authors: Tommaselli Giovanni A. , Di Carlo Costantino , Bifulco Giuseppe , Di Spiezio Sardo Attilio , Pellicano Massimiliano , Nappi Carmine 
Published: November 2003

Summaryobjective  Leptin seems to regulate reproductive function and it has been hypothesised that its secretion may be induced by oestrogens. Changes in its levels has been advocated as a determinant in the pathogenesis of premenstrual syndrome (PMS). We evaluated serum leptin levels in patients affected by PMS and in controls to establish: (i) if induced hypoestrogenism has an impact on leptin concentrations; (ii) if the administration of tibolone modifies the effects of hypoestrogenism on serum leptin levels; and (iii) if the improvement in PMS symptomatology can be correlated to changes in serum leptin levels.design  Prospective, randomized study.patients  Twenty‐eight women affected by PMS and 20 unaffected controls. Affected patients were randomly assigned to two groups to receive leuprolide acetate (3·75 mg intramuscularly) plus tibolone (2·5 mg/day) (group A; n = 14) or plus placebo (group B; n = 14), at the onset of the vasomotor symptoms.measurements  Serum leptin, oestradiol and progesterone levels, PMS signs and symptoms evaluated during a 2 months’ pretreament period and after 2 months of therapy.results  No differences in leptin levels among the three groups and within the same group at all time evaluated were observed. Oestradiol and progesterone concentrations were significantly lower in all groups during treatment in comparison with pretreatment values. Before therapy, leptin levels were positively correlated both with oestradiol and progesterone in the follicular and luteal phase in all groups. This correlation was lost after treatment. All PMS patients showed a significant improvement of the symptomatology.conclusions  Hypoestrogenism induced by GnRH analogues (GnRHa) does not seem to influence leptin levels in normal women and those with PMS, and the addition of tibolone does not impact on these levels. Because PMS symptomatology did significantly improve during treatment with GnRHa alone, or in associtation with tibolone, it is unlikely that changes in leptin levels could have an important role in the pathophysiology of PMS.
Acquired prolactin deficiency indicates severe hypopituitarism in patients with disease of the hypothalamic–pituitary axis
Authors: Mukherjee Annice , Murray Robert D. , Columb Breeda , Gleeson Helena K. , Shalet Stephen M. 
Published: November 2003

Summaryobjective  Prolactin deficiency has been the subject of many scientific studies, but there is a paucity of information regarding prolactin deficiency in humans. In this report, adults with disease of the hypothalamic–pituitary axis (HPA) were studied to determine the prevalence of severe acquired prolactin deficiency (APD) and the pathophysiological characteristics associated with it.patients and methods  APD was defined as a serum prolactin level persistently below the detection limit of the assay, i.e. less than 50 mU/l (normal range: male 85–444, female 85–530). Patients with a diagnosis of acromegaly, prolactinoma or with congenital or drug induced prolactin deficiency were excluded. Three hundred and sixty‐nine patients (190 women, age range 17–79 years) with disease of the HPA, meeting the specified criteria were identified.results  Twenty‐two (13 women, age range 29–76 years), showed evidence of APD. Thirteen of the 22 patients with APD had been treated for Cushing's disease. In all, 62 patients treated for Cushing's disease were identified, resulting in a prevalence of APD in treated Cushing's disease of 20·97%. Excluding treated Cushing's disease, the prevalence of APD in the remainder of the cohort was 2·93%. Nineteen patients with APD (86·4%) and 183 without APD (52·7%) underwent surgery in the region of the HPA (P = 0·0042). In contrast, nine patients with APD (40·9%) and 283 without APD (80·4%) had received radiotherapy, with fields which included the HPA (P < 0·001). No patient with isolated APD was identified. All patients with APD had evidence of severe GH deficiency (GHD) with a peak GH response to provocative stimuli of < 1·6 mU/l and a median IGF‐I standard deviation score (SDS) of −4·85 (quartiles −9·56 to −2·80). Of the 13 patients with APD and Cushing's disease, all were gonadotrophin and TSH‐deficient, six were adrenocorticotropic hormone (ACTH)‐deficient and six (46·1%) had cranial diabetes insipidus (CDI). Of the remaining nine patients with APD, total anterior pituitary hormone failure was present in all and CDI was present in two (22·2%).conclusions  The presence of APD indicates severe hypopituitarism in adults with HPA disease. It is universally associated with severe GHD. It is more common after surgery to the HP region. It has a low overall prevalence except in patients surgically treated for Cushing's disease.
Reduced exercise capacity in untreated adults with primary growth hormone resistance (Laron syndrome)
Authors: Ben‐Dov Issahar , Gaides Mark , Scheinowitz Mickey , Wagner Rivka , Laron Zvi 
Published: November 2003

Summaryobjective  Primary IGF‐I deficiency (Laron syndrome, LS) may decrease exercise capacity as a result of a lack of an IGF‐I effect on heart, peripheral muscle or lung structure and/or function.methods  Eight patients (six females) who had never received treatment with IGF‐I, with mean age of 36 ± 10 (SD) years (range 21–48), weight 47 ± 9 kg (31–61), height 126 ± 12 cm (112–140) and body mass index of 29 ± 4 kg/m2 (24–34), and 12 age‐matched controls, underwent lung function tests and incremental cycling to the limit of tolerance (CPX, MedGraphics). Predicted values for the patients were derived from adult equations based on height.results  In LS patients, lung function was near normal; vital capacity was 84 ± 11% of expected (66–103). Peak exercise O2‐uptake and the anaerobic threshold were reduced, 57 ± 20% of predicted and 33 ± 9% of predicted peak (P = 0·005 vs. controls), despite normal mean exercise breathing reserve. All parameters were normal in the controls.conclusion  Exercise capacity in untreated adults with LS is significantly reduced. The limitation for most patients was not ventilatory but resulted either from low cardiac output and/or from dysfunction of the peripheral muscles. However, the relative contribution of each of these elements and/or the role of poor fitness needs further study.