bluuebunny/crossref_metadata_2025_split huggingface dataset:
Is the conservative management of chronic retention in men ever justified?
Authors: Bates T.S. , Sugiono M. , James E.D. , Stott M.A. , Pocock R.D. 
Published: September 2003

OBJECTIVETo assess the outcome of men presenting with lower urinary tract symptoms (LUTS) associated with large postvoid residual urine volumes (PVR).PATIENTS AND METHODSThe study included men presenting with LUTS and a PVR of > 250 mL who, because of significant comorbidity, a low symptom score or patient request, were managed conservatively and prospectively, and were followed with symptom assessment, serum creatinine levels, flow rates and renal ultrasonography. Patients were actively managed if there was a history of previous outflow tract surgery, prostate cancer, urethral strictures, neuropathy, elevated creatinine or hydronephrosis. In all, 93 men (mean age 70 years, range 40–84) with a median (range) PVR of 363 mL (250–700) were included in the study and followed for 5 (3–10) years. At presentation, the median maximum flow rate was 10.2 (3–30) mL/s and the voided volume 316 (89–714) mL.RESULTSThe measured PVR remained stable in 47 (51%), reduced in 27 (29%) and increased in 19 (20%) patients; 31 patients (33%) went on to transurethral resection of the prostate after a median of 30 (10–120) months, because of serum creatinine elevation (two), acute retention (seven), increasing PVR (eight) and worsening symptoms (14). Of 31 patients 25 were available for evaluation after surgery; their median PVR was 159 (0–1000) mL, flow rate 18.4 (4–37) mL/s and voided volume 321 (90–653) mL. Symptoms were improved in all but five men. There was no difference in initial flow rate, voided volume or PVR between those who developed complications or went on to surgery and those who did not. Urinary tract infections (UTIs) occurred in five patients and two developed bladder stones.CONCLUSIONSComplications such as renal failure, acute retention and UTIs are uncommon in men with large, chronic PVRs. Conservative management for this group of patients is reasonable but outpatient review is prudent. There were no factors that could be used to predict those patients who eventually required surgery.
Quality of care for patients with Type 2 diabetes mellitus—a long‐term comparison of two quality improvement programmes in the Netherlands
Authors: Renders C. M. , Valk G. D. , De Sonnaville J. J. J. , Twisk J. , Kriegsman D. M. W. , Heine R. J. , Van Eijk J. Th. M. , Van Der Wal G. 
Published: September 2003

AbstractAim  To compare two intervention programmes, aimed at improving the quality of care provided for patients with Type 2 diabetes in the longer term.Methods  A retrospective comparison of data derived from two non‐randomized trials with 3.5 years of follow‐up. In the first intervention group 401 patients were included, 413 in the second intervention group and 105 in the reference group. The first programme focused on improving the skills and knowledge of general practitioners (GPs) with regard to Type 2 diabetes, and supported them in making organizational changes in their practice (GP care only). Centralized shared diabetes care was implemented in the second programme in which the GPs received therapy advice according to a protocol for each individual patient. The patients were also encouraged in self‐management, and received structured diabetes education (Diabetes Service). The main patient outcomes were HbA1c, blood pressure and serum lipid levels. Multilevel analysis was applied to adjust for dependency between repeated observations within one patient and for clustering of patients within general practices.Results  The HbA1c levels of patients of GPs who were supported by the Diabetes Service improved significantly more than the HbA1c levels of patients receiving GP care only {−0.28%[95% confidence interval (CI) −0.45; −0.11]}. In contrast, the systolic blood pressure of patients receiving GP care only decreased more than that of patients of GPs supported by the Diabetes Service [4.14 mmHg (95% CI 1.77, 6.51)].Conclusion  A Diabetes Service, providing GPs with individual therapy advice and patient education, resulted in better glycaemic control over 3.5 years than an intervention aimed at improving the skills of GPs in combination with organizational changes in the general practice.
Screening for diabetic retinopathy: a cause for concern in people who drive
Authors: Razvi S. , Myers L. , Patton K. , McCulloch A. J. 
Published: September 2003

AbstractAims  To report a case of a road traffic accident in a lady driving home from a diabetes clinic after pupillary dilatation. We also present the findings of a questionnaire survey of health professionals to elicit their practice in dealing with such patients.Methods  We present the case report of a lady having a road traffic accident on her way back from a retinal screening appointment after having had pupillary dilatation. A subsequent postal questionnaire survey was undertaken to find out current practice in screening patients who drive on the day of their retinal screening.Results  A lady was involved in a road traffic accident whilst returning home after retinal screening. Her motor insurance company refused to cover subsequent claims for damage because her pupils had been dilated. She was also prosecuted by the police for driving without valid motor insurance. We conducted a postal survey of 500 health care workers including ophthalmologists, optometrists, diabetologists and general practitioners regarding the use of dilating drops in people with diabetes who intend to drive. Analysis of 320 valid responses confirmed that there is no consistent practice with regard to either the use of dilating drops in drivers or in ensuring that arrangements are made for subsequent adequate visual inspection in those whom dilatory drops are not instilled.Conclusions  Guidelines, for use by health care professionals and people with diabetes, are clearly required regarding the use of pupillary dilating drops in drivers.
Insulin and lysophosphatidylcholine synergistically stimulate NO‐dependent cGMP production in human endothelial cells
Authors: Konopatskaya O. , Whatmore J. L. , Tooke J. E. , Shore A. C. 
Published: September 2003

AbstractAims  Nitric oxide (NO) is an important regulator of cardiovascular homeostasis. Lysophosphatidylcholine (lyso‐PC), a major constituent of oxidized low density lipoproteins (oxLDL), has been reported to impair nitric oxide‐dependent vasodilatation. This study investigated the possible mechanism of the lyso‐PC effect on insulin‐stimulated NO‐dependent of cyclic guanosine 3′,5′‐monophosphate (cGMP) generation in human endothelial cells.Methods  The intracellular concentration of cGMP in cultured human umbilical vein endothelial cells (HUVECs) was used to estimate NO production. The levels of endothelial nitric oxide synthase (eNOS) protein expression were assessed by Western blotting analyses.Results  Both insulin, at physiological concentration, and lyso‐PC stimulated rapid and prolonged intracellular of cGMP production, and together induced a marked synergistic response (for short‐term stimulation: 1185 ± 285.9% over control level (100%) compared with insulin and lyso‐PC alone (384.8 ± 67.4% and 357 ± 205%, respectively; P < 0.001), for long‐term stimulation: 3495 ± 1377%, compared with insulin and lyso‐PC alone (663 ± 131% and 487 ± 250%, P = 0.002)). Stimulated levels of cGMP accumulation were completely abrogated by NOS inhibitor, indicating NO involvement in the effects of insulin and lyso‐PC. Stimulated NO synthesis was not associated with altered eNOS protein expression. Cell subfractionation studies demonstrate that insulin and lyso‐PC each alone induced translocation of eNOS from the membrane to the cytosolic compartment and together caused a synergistic translocation.Conclusions  The presented data suggest that insulin and lyso‐PC synergistically upregulate endothelial NO production via eNOS translocation from the membrane fraction to the cytosol. This study raises the possibility that an interplay between various factors accompanying diabetes can lead to endothelial NO overproduction or desensitization of NO‐dependent responses. Appropriate rather than necessarily high levels of nitric oxide is the determinant of vascular health.
The ultrasound assessment of adipose tissue deposition in fetuses of ‘well controlled’ insulin‐dependent diabetic pregnancies
Authors: Greco P. , Vimercati A. , Hyett J. , Rossi A. C. , Scioscia M. , Giorgino F. , Loverro G. , Selvaggi L. 
Published: September 2003

AbstractObjective  To assess differences in adipose deposition in fetuses from normal pregnancies and women with diabetes.Research design and methods  The study group consisted of 15 well controlled insulin‐dependent women with diabetes and 16 controls with a normal glucose. Ultrasound measurements were taken of subcuticular tissue thickness at the abdominal and suprascapular level at 31 and 37 weeks gestation. Triceps and subscapular skinfold thickness were also measured at birth.Results  Gestational age at delivery and birthweights were not significantly different. At 31 weeks, fasting glucose levels were 5.0 ± 1 mmol/l for diabetic vs. 3.3 ± 0.3 mmol/l for controls (P < 0.01), post‐prandial 5.6 ± 0.4 vs. 5.1 ± 0.3 mmol/l (P < 0.01). At 37 weeks, they were 4.6 ± 0.2 mmol/l vs. 3.8 ± 1.1 mmol/l (P < 0.01) and 6.0 ± 0.6 mmol/l vs. 5.3 ± 0.3 mmol/l (P < 0.01). Abdominal and suprascapular subcuticular thickness were 4.4 ± 0.1 mm vs. 3.7 ± 0.1 mm (P < 0.05) and 4.3 ± 0.2 mm vs. 3.5 ± 0.2 mm (P < 0.05) at 31; 5.6 ± 0.2 mm vs. 4.8 ± 0.1 mm (P < 0.05) and 5.4 ± 0.2 mm vs. 4.4 ± 0.1 mm (P < 0.05) at 37 weeks. At birth, triceps and suprascapular skinfolds were 4.7 ± 0.1 mm vs. 4.1 ± 0.1 mm (P < 0.05) and 4.7 ± 0.2 mm vs. 3.8 ± 0.1 mm (P < 0.01).Conclusion  Adipose tissue disposition is increased in fetuses of women with well‐controlled diabetes. This may be a reflection of higher maternal glucose levels in these women and may explain why even well‐controlled diabetic pregnancies are at risk of macrosomia.
Serum leptin is elevated in Saudi Arabian patients with metabolic syndrome and coronary artery disease
Authors: Al‐Daghri N. , Al‐Rubean K. , Bartlett W. A. , Al‐Attas O. , Jones A. F. , Kumar S. 
Published: September 2003

AbstractAims  To compare plasma leptin in Saudi subjects with Type 2 diabetes and coronary heart disease (CHD) with non‐diabetic control subjects and to examine the relationship of plasma leptin to other CHD risk factors.Research design and method  Serum leptin concentrations were measured in 144 Saudi men. Subjects studied included 59 with Type 2 diabetes mellitus [BMI 27.5 (3.7) kg/m2 mean (sd)], 34 with coronary heart disease [BMI 29.6 (1.8) kg/m2], and 51 non‐diabetic controls [BMI 28.0 (3.5) kg/m2]. There was no significant difference in BMI between the groups. Fasting serum leptin, lipids, insulin, apolipoproteins and glucose were measured. BMI, blood pressure; smoking habit and age were also recorded. Insulin resistance was assessed using the HOMA model.Results  Leptin concentrations were significantly higher in diabetic and CHD patients than in controls (P = 0.024 and 0.016, respectively). Multiple regression analysis showed that body weight (P < 0.0006), serum triglyceride concentration (P = 0.046) and systolic blood pressure (P = 0.013) were all significantly related to the logarithm of the serum leptin concentration (R2 = 0.549) in CHD patients. A subgroup analysis, comparing those patients who had the metabolic syndrome, as defined by WHO, with controls, showed higher serum leptin in those with metabolic syndrome (P = 0.05).Conclusions  Serum leptin is increased in Saudi subjects with diabetes mellitus, metabolic syndrome and CHD. Leptin may be a marker of risk of CHD, at least in men, and contribute to the CHD risk profile in subjects with insulin resistance. Further studies are needed to evaluate this relationship prospectively.
Serum resistin level in essential hypertension patients with different glucose tolerance
Authors: Zhang J.‐L. , Qin Y.‐W. , Zheng X. , Qiu J.‐L. , Zou D.‐J. 
Published: September 2003

AbstractAims  To investigate resistin concentrations in patients with essential hypertension and different glucose tolerance and the relationship between serum resistin level and blood glucose.Methods  Sixty‐five patients with essential hypertension [13 with Type 2 diabetes mellitus (DM), 26 with impaired glucose tolerance (IGT), and 26 with normal glucose tolerance (NGT); 30 males, 35 females] were studied. Fasting serum resistin concentrations were measured by enzyme immunoassay (EIA). Oral glucose tolerance tests and insulin release tests were used to calculate glucose area under the curve (AUCG), the ratio of insulin to glucose (ΔI30/ΔG30), and insulin sensitivity index (ISI) according to Cederholm's formula.Results  Fasting serum resistin concentrations (µg/l) in DM (34.9 ± 10.2) patients were significantly higher than those in IGT (25.1 ± 10.4) (P < 0.05) and in NGT (21.5 ± 7.9) (P < 0.05) patients. Pearson correlation showed that fasting serum resistin concentration was correlated with AUCG (r = 0.445, P < 0.001), ISI (r = −0.322, P < 0.01) and ΔI30/ΔG30 (r = −0.366, P < 0.01), but not body mass index and waist‐hip ratio. After adjustment for gender, age and body mass index (BMI), partial correlation analysis showed that the fasting serum resistin concentrations were still correlated with AUCG (r = 0.327, P < 0.01) and ΔI30/ΔG30 (r = −0.348, P < 0.01), but ISI.Conclusion  Resistin may be involved in the development of diabetes in humans.
A qualitative investigation of the views and health beliefs of patients with Type 2 diabetes following the introduction of a diabetes shared care service
Authors: Smith S. M. , O'Leary M. , Bury G. , Shannon W. , Tynan A. , Staines A. , Thompson C. 
Published: September 2003

AbstractAims  A qualitative research approach was adopted in order to explore the views and health beliefs of patients with Type 2 diabetes who had experienced a new structured diabetes shared care service.Methods  Patients from 15 general practices were randomly selected and invited to attend three focus groups. Two independent researchers adopted the ‘Framework’ technique to analyse the transcribed data and identify key themes expressed by patients.Results  Themes relating to diabetes included frustration, victimization and powerlessness in relation to living with diabetes, controlling blood sugar, medication and economic barriers to care. Differences in emphases between patients and healthcare providers emerged. Patients were generally positive about shared care and largely identified it with the nurses involved.Conclusion  This research highlights the importance of an in‐depth exploration of patients’ views during changes in diabetes care delivery to identify service delivery failures and gaps in patient knowledge such as lack of awareness of the extent of macrovascular risk.
Recovery of brain docosahexaenoate leads to recovery of spatial task performance
Authors: Moriguchi Toru , Salem Norman 
Published: September 2003

AbstractInfants fed vegetable oil‐based formulas may have poorer visual function, lower cognitive scores and acquire learning tasks more slowly in comparison with those breast fed or those fed formulas supplemented with docosahexaenoate. The aim of the present study was to determine the reversibility of losses in brain function associated with the loss of brain DHA. Rats were fed very low or adequate levels of n‐3 fatty acids through three generations. The n‐3 fatty acid deficient animals of the F3 generation were then given an n‐3 adequate diet containing alpha‐linolenic and docosahexaenoic acids (DHA) at birth, weaning (3 weeks) or young adulthood (7 weeks). The spatial task performance of these animals returned to the n‐3 adequate diet was then compared using the Morris water at two different ages, at 9 or 13 weeks. Our results indicate that animals repleted since birth or at weaning were able to achieve nearly the same level of brain DHA and spatial task performance as animals maintained for three generations on an n‐3 adequate diet. In the case of young adult animals, the degree of DHA and behavioral performance recovery depended upon the duration of dietary repletion with substantial recovery in animals after 6 weeks but little recovery of function after two weeks. The significance of these findings is that they indicate that at least some of the adverse effects of DHA deficiency during neurodevelopment may be reversible with an n‐3 fatty acid supplemented diet.
On high‐ and low‐affinity agonist sites in GABAA receptors
Authors: Baur Roland , Sigel Erwin 
Published: September 2003

AbstractGABAA receptors are activated via low‐affinity binding sites for the agonists GABA or muscimol. Evidence has been provided that the amino acid residueα1F64 located at the β2(+)/α1(–) subunit interface forms part of this binding site. In radioactive ligand binding studies the agonist [3H]muscimol has been found to interact with the receptor via a high‐affinity binding site. This site has been interpreted as a conformational variant of the low‐affinity site. Alternatively, the high‐affinity binding site has been located to the α1(+)/β2(–) interface and the homologous residue to α1F64, β2Y62 has been proposed to constitute an important part of this site. Here we investigated the effect of the point mutation α1F64L and the homologous mutation β2Y62L on agonist and antagonist binding and functional properties in α1β2γ2 GABAA receptors. While the mutation in the α1 subunit had drastic consequences on all studied properties, including desensitization, the mutation in the β2 subunit had little consequence. Our observations are relevant for the relative location of high‐ and low‐affinity agonist sites in GABAA receptors.
Changes in cortical acetyl‐CoA metabolism after selective basal forebrain cholinergic degeneration by 192IgG‐saporin
Authors: Tomaszewicz Maria , Roßner Steffen , Schliebs Reinhard , Ćwikowska Justyna , Szutowicz Andrzej 
Published: September 2003

SummaryThe aim of the present study was to reveal whether reduced cortical cholinergic input affects the acetyl‐CoA metabolism in cholinoceptive cortical target regions which may play a causative role for the deficits in cerebral glucose metabolism observed in Alzheimer's disease. The effect of cortical cholinergic denervation produced by a single intracerebroventricular application of the cholinergic immunotoxin 192IgG‐saporin, on activities of pyruvate dehydrogenase and adenosine triphosphate (ATP)‐citrate lyase as well as on the level of synaptoplasmic and mitochondrial acetyl‐CoA and acetylcholine release in cortical target regions was studied. Cholinergic lesion produced 83%, 72% and 32% decreases in the activities of choline acetyltransferase, acetylcholinesterase and ATP‐citrate lyase in nerve terminals isolated from rat brain cortex, respectively, but no change in pyruvate dehydrogenase activity. Spontaneous and Ca2+‐evoked acetylcholine release from synaptosomes was inhibited by 76% and 73%, respectively, following immunolesion. The lesion‐induced 39% decrease of acetyl‐CoA level in synaptosomal mitochondria was accompanied by 74% increase in synaptoplasmic fraction. Levels of acetyl‐CoA and CoASH assayed in fraction of whole brain mitochondria from lesioned cortex were 61% and 48%, respectively, higher as compared to controls. The data suggest a preferential localization of ATP‐citrate lyase in cholinergic nerve terminals, where it may contribute to the transport of acetyl‐CoA from the mitochondrial to the cytoplasmic compartment. They provide evidence on differential distribution of acetyl‐CoA in subcellular compartments of cholinergic and non‐cholinergic nerve terminals. There are also indications that cholinergic activity affects acetyl‐CoA level and its intracellular distribution in glial and other non‐cholinergic cortical cells.
P2X7 nucleotide receptor activation enhances IFNγ‐induced type II nitric oxide synthase activity in BV‐2 microglial cells
Authors: Gendron Fernand‐Pierre , Chalimoniuk Malgorzata , Strosznajder Joanna , Shen Siming , González Fernando A. , Weisman Gary A. , Sun Grace Y. 
Published: September 2003

AbstractUnder normal and pathological conditions, brain cells release nucleotides that regulate a wide range of cellular responses due to activation of P2 nucleotide receptors. In this study, the effect of extracellular nucleotides on IFNγ‐induced NO release in murine BV‐2 microglial cells was investigated. BV‐2 cells expressed mRNA for metabotropic P2Y and ionotropic P2X receptors. Among the P2 receptor agonists tested, ATP, ADP, 2′,3′‐O‐(4‐benzoylbenzoyl)‐ATP (BzATP), and 2‐methylthio‐ATP (2‐MeSATP), but not UTP, enhanced IFNγ‐induced iNOS expression and NO production, suggesting that the uridine nucleotide receptors P2Y2 and P2Y6 are not involved in this response. U0126, an antagonist for MEK1/2, a kinase that phosphorylates the extracellular signal‐regulated kinases ERK1/2, decreased IFNγ‐induced NO production. BzATP, a potent P2X7 receptor agonist, was more effective than ATP, ADP, or 2‐MeSATP at enhancing IFNγ‐induced ERK1/2 phosphorylation. Consistent with activation of the P2X7 receptor, periodate‐oxidized ATP, a P2X7 receptor antagonist, and suramin, a non‐specific P2 receptor antagonist, inhibited the effect of ATP or BzATP on IFNγ‐induced NO production, whereas pyridoxal‐phosphate‐6‐azophenyl‐2′,4′‐disulfonic acid (PPADS), an antagonist of several P2X receptor subtypes, was ineffective. These results suggest that activation of P2X7 receptors may contribute to inflammatory responses in microglial cells seen in neurodegenerative diseases.
Copper and zinc cause delivery of the prion protein from the plasma membrane to a subset of early endosomes and the Golgi
Authors: Brown Lesley R. , Harris David A. 
Published: September 2003

AbstractThe cellular isoform of prion protein (PrPC) is a plasma membrane glycoprotein whose conformational conversion into PrPSc is the central molecular event in the propagation of infectious prions. However, the physiological function of PrPC has remained uncertain. The finding that PrPC binds copper ions with low micromolar affinity, coupled with several other observations, has led to the proposal that the protein plays a role in copper homeostasis. Using biochemical techniques, we had shown previously that copper ions rapidly and reversibly stimulate endocytosis of PrPC from the cell surface. In this report, we employ immunofluorescence microscopy to further investigate the specificity and kinetics of metal effects on PrPC trafficking and to identify the intracellular compartments to which internalized PrPC is delivered in response to copper and zinc. We find that both of these metals stimulate redistribution of surface PrPC to a subset of transferrin‐containing early endosomes as well as to Golgi compartments. These results are consistent with models in which PrPC plays a role in the cellular uptake or efflux of transition metals.