bluuebunny/crossref_metadata_2025_split huggingface dataset:
Low plasma levels of dehydroepiandrosterone sulphate in HIV‐positive patients coinfected with hepatitis C virus
Authors: Mauboussin JM , Mahamat A , Peyrière H , Rouanet I , Fabbro‐Peray P , Daures JP , Vincent D 
Published: May 2004

ObjectivesTo evaluate plasma levels of dehydroepiandrosterone sulphate (DHEAS) in a cohort of HIV‐infected patients and to analyse factors associated with DHEAS levels.MethodsWe conducted a cross‐sectional survey in the Nîmes University Hospital cohort of HIV‐infected patients in south‐eastern France. All HIV‐infected patients with at least one outpatient visit between 1 January and 1 September 2002 were included in the study. Sociodemographic, clinical, therapeutic, immuno‐virological and plasma DHEAS level data were collected during this period. Hepatitis C virus (HCV) coinfection was defined as the presence of HCV antibody with positive RNA. To identify factors associated with plasma DHEAS levels, Spearman's rank correlation and univariate and multivariate linear regression analyses were used.ResultsThe DHEAS plasma level was measured in 137 patients (104 men and 33 women), 37 (27.0%) of whom were HCV coinfected. The median age of the patients was 39.1 years [interquartile range (IQR): 34.9–48.7] for women and 41.8 years (36.5–47.7) for men. The median DHEAS level was 5.5 μmol/L (IQR: 2.3–8.8) for the whole sample of 137 patients, and was lower in women (2.4 μmol/L; 1.5–6.6) than in men (6.1 μmol/L; 2.5–9.0) (P<0.01), and lower in patients coinfected with HCV (2.1 μmol/L; 0.6–6.7) than in those not coinfected (6.6 μmol/L; 3.0–9.1) (P<0.01). Of all prognostic factors studied in the variance covariance analysis, three factors were associated with DHEAS: age, gender and HCV coinfection. Subgroup analysis revealed that the age‐adjusted mean of the DHEAS level was lower in HCV coinfected patients for both women (1.3±1.1 μmol/L) and men (4.0±0.7 μmol/L), compared with patients not HCV coinfected (women, 5.3±0.7 μmol/L; men, 7.2±0.4 μmol/L) (P<0.01).ConclusionsThis is the first report of the determination of DHEAS plasma levels in HIV/HCV coinfected patients. When age and sex were taken into account, the DHEAS plasma level was found to be significantly lower in HCV coinfected patients. To date, the pathophysiology of such findings is unknown.
Castleman's disease and HIV infection in Australia
Authors: Loi S , Goldstein D , Clezy K , Milliken ST , Hoy J , Chipman M 
Published: May 2004

ObjectivesTo describe, retrospectively, the Australian experience of muti‐centric Castleman's disease (MCD) in the setting of HIV infection, specifically with the advent of HAART, and newer chemotherapeutic agents.Patients and methodsHIV‐infected patients diagnosed with MCD since 1994, were identified from three major HIV treatment centres in Australia. Demographic and disease characteristic variables were collated by the National Centre in HIV Epidemiology and Clinical Research.ResultsEleven patients were identified with MCD. Medial follow up was 46 (18–57) months. All had CD4 cell counts less than 500 cells/μL. All but one patient was receiving HAART at the time of diagnosis. Nine of the 11 patients had Kaposi's sarcoma (KS) and two patients also developed non‐Hodgkin's Lymphoma (NHL). All patients received chemotherapy for MCD. The response rate from Chemotherapy was 64%. Only two patients achieved sustained remissions. The median survival was 21.9 (1–52) months. The mortality was 45% from MCD and its related complications.ConclusionMCD in HIV infected patients is a rare and life‐threatening disorder. There is limited recent information on optimal treatment for MCD. MCD in our series appeared to be a chemo‐responsive disease. In our experience, treatment with liposomal anthracycline was associated with good response rates and acceptable toxicity in several patients, and therefore merits further exploration to establish its role. Treatment in the future may concentrate on novel agents such as anti‐interleukin 6, anti‐CD20 antibodies, thalidomide and viral ablation.
The AIDS epidemic in Lyon: patient characteristics and defining illnesses between 1985 and 2000
Authors: Gayet‐Ageron A , Baratin D , Marceillac E , Allard R , Peyramond D , Chidiac C , Trepo C , Livrozet J‐M , Touraine J‐L , Ritter J , Sepetjan M , Fabry J , Vanhems P 
Published: May 2004

ObjectivesTo define the characteristics of 1899 patients diagnosed with AIDS at Lyon University Hospitals (LUH) across four time periods corresponding to different antiretroviral eras, and to analyse the evolution of specific AIDS‐defining illnesses (ADIs) with time.MethodsAll AIDS patients at LUH between 1 January 1985 and 31 December 2000 were included in the study. The data were compared using the χ2 test and one‐way analysis of variance.ResultsThe absolute number of new AIDS cases increased by 30.3% between 1985 and 1995 but decreased by 26.5% between 1996 and 2000. The proportion of women with AIDS increased significantly (P<0.001) and mean age at diagnosis also increased significantly over time (P<0.001). The proportion of infection through heterosexual contact increased dramatically, while that through homo/bisexual intercourse or injection drug use (IDU) decreased significantly (P<0.001). The absolute number of ADIs declined with the introduction of highly active antiretroviral therapies (HAART) (P<10–6). Pneumocystis carinii pneumonia remained the leading ADI in 1996–2000 (23.3%). A significant increase in the proportion of non‐Hodgkin's lymphoma (NHL) was observed over time (P<10–5) but the number of new NHL cases decreased during HIV infection after 1996.ConclusionsThe decline in the incidence of AIDS with the advent of HAART was confirmed in our hospital cohort. The gradual increase in the proportion of NHL among ADIs underscores the long latency period between infection with HIV and the achievement of an effect of HAART on HIV‐associated lymphomagenesis.
Isolated antibodies against the core antigen of hepatitis B virus in HIV‐infected patients
Authors: Neau D , Winnock M , Galpérine T , Jouvencel AC , Castéra L , Legrand E , Tranchant E , Balestre E , Lacoste D , Ragnaud JM , Dupon M , Lafon ME , Dabis F ,   for the Groupe d'Epidémiologie Clinique du SIDA en Aquitaine (GECSA)
Published: May 2004

SummaryThe aim of this study was to describe the frequency and significance of isolated antibodies against the hepatitis B virus (HBV) core antigen (HBc) in 2185 HIV‐infected patients of the Aquitaine Cohort. Antibodies against HBc were found in 372 subjects (17%). Patients with isolated anti‐HBc antibodies were more frequently coinfected with hepatitis C virus (HCV) (58.2%) than those who were anti–HB surface (HBs) antibody positive (22.9%, P<0.001) and those who were dually reactive anti‐HBs/anti‐HBc antibody positive (27.3%, P<0.001). These results suggest interactions between HBV and HCV. As observed in patients not infected with HIV, the ‘anti‐HBc‐alone’ serological profile could reflect essentially late immunity with undetectable anti‐HBs antibodies. However, an occult HBV infection cannot be ruled out.
HIV and hepatitis C coinfection within the CAESAR study
Authors: Amin J , Kaye M , Skidmore S , Pillay D , Cooper DA , Dore GJ 
Published: May 2004

SummaryThe declining incidence of AIDS‐related opportunistic diseases among people with HIV infection has shifted the focus of clinical management to prevention and treatment of comorbidities such as chronic liver disease. The increased risk of hepatitis C virus (HCV)‐related advanced liver disease in people with HIV infection makes early HCV diagnosis a priority. To assess HCV prevalence and predictors of HIV/HCV coinfection, we have conducted a retrospective analysis of people enrolled in the CAESAR (Canada, Australia, Europe, South Africa) study, a multinational randomized placebo‐controlled study of the addition of lamivudine to background antiretroviral therapy. The impact of HCV on HIV disease progression was also examined. Anti‐HCV antibody testing on 1649 CAESAR study participants demonstrated a HIV/HCV coinfection prevalence of 16.1%, which varied from 1.9% in South Africa to 48.6% in Italy. The strongest predictor of HIV/HCV coinfection was HIV exposure category (P<0.0001), with odds ratios (ORs) compared to homosexual as follows: injecting drug use (IDU), 365 [95% confidence interval (CI): 179–742]; transfusion or blood products, 32.2 (95% CI: 15.2–67.6); homosexual and IDU, 22.9 (95% CI: 8.5–62.1). The prevalence of HIV/HCV was low (3.7%) among homosexual men without reported IDU. Other predictors of HIV/HCV coinfection were alanine aminotransferase (ALT), country of residence, ethnicity and stage of HIV disease. A history of IDU or ALT ≥40 U/L at baseline had a positive predictive value (PPV) of 35%, negative predictive value (NPV) of 96%, sensitivity of 82% and specificity of 71% for HIV/HCV coinfection. HIV disease progression was similar in HIV monoinfected and HIV/HCV coinfected patients. People with HIV and a history of IDU or elevated liver function tests should be targeted for HCV testing. The low prevalence of HIV/HCV coinfection among homosexual men without a history of IDU suggests low efficiency of sexual HCV transmission.
Clinical implications of stopping nevirapine‐based antiretroviral therapy: relative pharmacokinetics and avoidance of drug resistance
Authors: Mackie NE , Fidler S , Tamm N , Clarke JR , Back D , Weber JN , Taylor GP 
Published: May 2004

ObjectiveTo determine the pharmacokinetics of cessation of nevirapine (NVP) in order to design clinical protocols which will reduce the risk of resistance to nonnucleoside reverse transcriptase inhibitors (NNRTIs).MethodsIn a case study, NNRTI genotypic resistance was demonstrated in a patient discontinuing therapy for toxicity. Subsequently, nine patients receiving NVP‐containing antiretroviral regimens and stopping treatment were recruited. Patients were advised to continue the nucleoside analogue reverse transcriptase inhibitor (NRTI) backbone for 5 days following cessation of NVP. Plasma NVP concentrations were determined over 7–10 days after the last dose. HIV‐1 reverse transcriptase genotyping was performed at viral load rebound (approximately day 21 following cessation) to detect mutations associated with reduced NNRTI sensitivity.ResultsThe median predicted time for plasma NVP concentration to fall below the inhibitory concentration (IC)50 of wild‐type virus was 168 h (range 108–264 h). De novo genotypic mutations conferring resistance to NRTIs or NNRTIs were not demonstrated following cessation of therapy.ConclusionsThe prolonged elimination half‐life of NVP compared with NRTIs, which persists even after 20 weeks of therapy, raises concern over the development of NNRTI resistance if all three drugs are stopped together. Continuation of the NRTI backbone for a further 5 days, allowing the elimination of NVP, may avoid the development of drug resistance.
Peyronie's disease in men with HIV responding to highly active antiretroviral therapy
Authors: Rogers GD , French MA 
Published: May 2004

SummaryThe pathogenesis of Peyronie's disease (induratio penis plastica) is unclear, but immune phenomena appear likely to be involved. Two cases are presented where the condition developed in temporal association with a virological response to highly active antiretroviral therapy (HAART) in men with HIV infection. It is suggested that this may represent another manifestation of immune restoration disease.
Accounting for change in public sector industrial relations: the erosion of national bargaining in further education in England and Wales
Authors: Williams Steve 
Published: May 2004

AbstractThe recent transformation of industrial relations in further education in England and Wales is examined, in particular the role of the national ‘Silver Book’ dispute over lecturers’ conditions of service in causing the erosion of national bargaining in the sector. The experience of further education points to the limits of the strategic choice approach as a device for explaining change in public sector industrial relations and to the importance of supplementing it with a perspective that emphasises the role of power.
Speeds of Actin Translocation in Vitro by Myosins Extracted from Single Rat Muscle Fibres of Different Types
Authors: Canepari M. , Rossi R. , Pellegrino M. A. , Reggiani C. , Bottinelli R. 
Published: May 2004

SUMMARYAs skeletal muscle fibres mostly express a single myosin isoform, they are a potential source of pure myosin isoforms. A technique is described that allows extraction and identification of pure myosin isoforms from single fibres, and testing of such myosins in an in vitro motility assay (IVMA). The results show that the extraction procedure does not alter myosin function and support the view that single fibres are reliable sources of purified myosin isoforms for IVMA.
Interaction of Islet Hormones with Cholecystokinin Octapeptide‐Evoked Secretory Responses in the Isolated Pancreas of Normal and Diabetic Rats
Authors: Singh Jaipaul , Adeghate Ernest , Salido Gines M. , Pariente Jose A. , Yago Maria D. , Juma Lubna O. M. 
Published: May 2004

SUMMARYThis study investigates the effects of the islet hormones, insulin (Ins), glucagon (Glu) and somatostatin (Som) with cholecystokinin octapeptide (CCK‐8) on amylase secretion and intracellular free calcium concentration [Ca2+]i and their pattern of distribution in the isolated pancreas of normal and diabetic rats. Ins and Glu evoked small increases in amylase output from pancreatic segments compared with a much enhanced effect of CCK‐8. In contrast, Som induced a biphasic response comprising an initial decrease followed by a secondary increase and this biphasic response may be dependent upon the concentration. Combining the islet hormones with CCK‐8 resulted in marked potentiation in amylase output compared with either CCK‐8 alone or the individual hormone. Genistein and tyrphostin A25, the tyrosine kinase inhibitors, evoked a small decrease in amylase output from pancreatic segments. They had no effect on the CCK‐8‐evoked secretory response but markedly inhibited the potentiation of the islet hormones with CCK‐8. In pancreatic acini and acinar cells Ins, Glu and Som individually evoked small increases in amylase output compared with a much larger response with CCK‐8. When the islet hormones were combined with CCK‐8 there was no potentiation of amylase output. Similarly, when rats were rendered diabetic by prior treatment with streptozotocin Ins, Glu and Som failed to potentiate the secretory response of CCK‐8. In fura‐2‐loaded pancreatic acinar cells Ins or Glu evoked small increases in [Ca2+]i compared with a much larger elevation with CCK‐8. Ins, Glu and Som each enhanced the CCK‐8‐evoked [Ca2+]i. Genistein elicited a decrease in [Ca2+]i both in the absence and presence of the islet hormones. It also decreased the elevation in [Ca2+]i resulting from the combined presence of CCK‐8 with either Ins or Glu but it had no effect on CCK‐8 in combination with Som. In pancreatic acinar cells from diabetic rat Ins, Glu and Som had no detectable effect on CCK‐8‐evoked elevation in [Ca2+]i compared with the response obtained with CCK‐8 alone. CCK‐8‐immunopositive cells were distributed around the walls of blood vessels, numerous Ins‐positive cells in the central and peripheral parts of the islets of Langerhans, Glu‐immunoreactive cells in the periphery of islets and Som‐positive cells in the outer part of the islets. During diabetes, the number of CCK‐immunopositive cells remained unchanged whereas the number of Ins‐positive cells decreased coupled with an increase in the number of Glu‐positive cells. The results indicate that both tyrosine kinase and cellular Ca2+ seem to be the intracellular mediators involved with the enhanced secretory responses obtained with a combination of the islet hormones with CCK‐8. Moreover, the presence of viable pancreatic islets of Langerhans seems to be associated with the potentiation of the islet hormones with CCK‐8.
Activation of Ionic Channels by Deoxycholate in Frog and Human Cell Lines
Authors: Maurício A. C. , Ferreira K. T. G. 
Published: May 2004

SUMMARYHumans, after extensive ileal resection, frequently suffer from diarrhoea, which may be due to an increased delivery of deoxycholate (DOC) to the large intestine. In the frog skin the addition of DOC (0·5 mM) to the apical side induced the activation of amiloride‐sensitive Na+ channels and an increase in the unidirectional Cl− fluxes. Here we used two established cell lines (A6 and Caco2) to study the effect of DOC on ion channels at cell and membrane level using the patch‐clamp technique. In A6 cells subcultured directly on Petri dishes and studied in the whole‐cell configuration, DOC induced an increase in cell conductance of 110·3 ± 4 pS pF−1 (N= 8) which was reduced to 89 ± 14 pS pF−1 (N= 8) by the addition of DIDS (0·5 mM). The absolute values of these two effects were not statistically different (P < 0·2). In Caco2 cells, the addition of DOC (0·5 mM) induced, after 1 min, an increase in cell conductance of 583 ± 16 pS pF−1 (N= 8) which was reduced to 560·4 ± 16 pS pF−1 (N= 8) by DIDS (0·5 mM) and N‐phenylanthranilic acid (DPC; 0·5 mM). The two values were not statistically different (P < 0·4). In Caco2 cells subcultured under the same conditions, DOC induced an increase in cell conductance of 1710 ± 64 pS pF−1 (N= 6). Subsequent addition of amiloride (0·1 mM) reduced the cell conductance to 1558 ± 33 pS pF−1 (N= 6). These two mean values were statistically different allowing for an error of the second kind < 0·05. In cells in which DOC produced a conductance increase of 1010 ± 10 pS pF−1, gadolinium (0·5 mM) induced a fall in cell conductance of 1800 ± 10 pS pF−1. In Caco2 cells, addition of DOC (0·5 mM) to the bath reversibly induced the appearance of or an increase in channel activity in patches studied in cell‐attached and excised inside‐out configuration. In inside‐out experiments (N= 13) DOC (0·5 mM) induced the appearance of channel activity with conductances and reversal potentials (Er) of 27·7 ± 1·9 pS and 0·8 ± 5·7 mV, respectively. In cell‐attached patches (N= 13) these values were 24·9 ± 4·4 pS and ‐18·1 ± 6·4 mV. In excised inside‐out patches from Caco2 cells, subjected to electrochemical gradients for Na+, K+ and Cl−, (+85, ‐85 and 0 mV, respectively), addition of DOC also induced an increase in the baseline conductance and a shift in the reversal potential from values around +25 mV to values around 0 mV. Bile salts activated both anionic and cationic channels and did not require the presence of intracellular factors for these effects. We suggest that they act at the membrane level.
Regulatory Role of cAMP in Transport of Na+, Cl− and Short‐Chain Fatty Acids Across Sheep Ruminal Epithelium
Authors: Gäbel Gotthold , Butter Heidrun , Martens Holger 
Published: May 2004

SUMMARYSodium is absorbed in considerable amounts across the ruminal epithelium, whilst its transport is strongly interrelated with the permeation of chloride and short‐chain fatty acids (SCFAs). However, regulation of ruminal Na+, Cl−, and SCFA absorption is hardly understood. The present study was therefore performed to characterize the influence of cAMP on sodium and sodium‐coupled transport mechanisms in short‐circuited, stripped ruminal epithelia of sheep. Elevation of intracellular cAMP concentrations by theophylline (10 mM) or theophylline in combination with forskolin (0·1 mM) significantly reduced mucosal‐to‐serosal sodium transport, leading to a reduction of net transport. The theophylline‐ or theophylline‐forskolin‐induced reduction of sodium transport was accompanied by a decrease in chloride net transport but revealed no effect on propionate flux. Short‐chain fatty acids stimulated Na+ transport but their stimulatory effect was almost completely blocked by theophylline‐forskolin. In solutions with and without SCFAs, the inhibitory effect of 1 mM amiloride on sodium transport was strongly reduced after theophylline‐forskolin pretreatment of the tissues. Blocking the production of endogenous prostaglandins by addition of indomethacin (10 μM) led to a theophylline‐sensitive stimulation of unidirectional and net fluxes of sodium. The findings indicate that apical, amiloride‐sensitive Na+‐H+ exchange and/or basolateral Na+‐K+‐ATPase can effectively be blocked by cAMP, leading to a decrease in sodium and chloride transport. In the ruminal epithelium, cAMP is a second messenger of prostaglandins, which are released spontaneously under in vitro conditions.
Drug Extrusion, 125I− Efflux and the Control of Intracellular [Ca2+] in Drug‐Resistant Ovarian Epithelial Cells
Authors: McAlroy H. L. , Bovell D. L. , Plumb J. A. , Thompson P. , Wilson S. M. 
Published: May 2004

SUMMARYExperiments were undertaken using an ovarian adenocarcinoma cell line (A2780) and a drug‐resistant strain (A2780.ad) derived from this line. P‐glycoprotein could not be detected in A2780 cells but was essentially ubiquitous in A2780.ad cells, although removing the selective pressure for drug resistance led to reduced expression. However, the amount of P‐glycoprotein present was used to predict the capacity of these cells to extrude rhodamine‐123 (R‐123) and their resistance to adriamycin, a cytotoxic drug. This accords with the role of P‐glycoprotein as a drug pump. Although hypotonic solutions increased anion efflux from A2780 and A2780.ad cells, larger responses occurred in the parental line. Moreover, R‐123 extrusion and anion efflux appeared to be mutually independent processes and so these data do not support the view that P‐glycoprotein is involved in the control of volume‐sensitive anion channels. Hypotonic solutions increased intracellular free calcium ([Ca2+]i) in drug‐resistant cells but not in the parental line, and so establishing a drug‐resistant strain may affect the control of [Ca2+]i during osmotic swelling. This could account for effects that were previously attributed to P‐glycoprotein.
The Effects of Caffeine on the Kinetics of O2Uptake, CO2Production and Expiratory Ventilation in Humans During the On‐Transient of Moderate and Heavy Intensity Exercise
Authors: Bell C. , Kowalchuk J. M. , Paterson D. H. , Scheuermann B. W. , Cunningham D. A. 
Published: May 2004

SUMMARYIn order to test the hypothesis that glycogen sparing observed early during exercise following caffeine ingestion was a consequence of tighter metabolic control reflected in faster VO2 kinetics, we examined the effect of caffeine ingestion on oxygen uptake (VO2), carbon dioxide production (VCO2) and expiratory ventilation (VE) kinetics at the onset of both moderate (MOD) and heavy (HVY) intensity exercise. Male subjects (n= 10) were assigned to either a MOD (50 % VO2,max, n= 5) or HVY (80 % VO2,max, n= 5) exercise condition. Constant‐load cycle ergometer exercise was performed as a step function from loadless cycling 1 h after ingestion of either dextrose (placebo, PLAC) or caffeine (CAFF; 6 mg (kg body mass)−1). Alveolar gas exchange was measured breath‐by‐breath. A 2‐ or 3‐component exponential model, fitted through the entire exercise transient, was used to analyse gas exchange and ventilatory data for the determination of total lag time (TLT: the time taken to attain 63 % of the total exponential increase). Caffeine had no effect on TLT for VO2 kinetics at either exercise intensity (MOD: 36 ± 14 s (PLAC) and 41 ± 10 s (CAFF); HVY: 99 ± 30 s (PLAC) and 103 ± 26 (CAFF) (mean ±s.d.)). TLT for VE was increased with caffeine at both exercise intensities (MOD: 50 ± 20 s (PLAC) and 59 ± 21 s (CAFF); HVY: 168 ± 35 s (PLAC) and 203 ± 48 s (CAFF)) and for VCO2 during MOD only (MOD: 47 ± 14 s (PLAC) and 53 ± 17 s (CAFF); HVY: 65 ± 13 s (PLAC) and 69 ± 17 s (CAFF)). Contrary to our hypothesis, the metabolic effects of caffeine did not alter the on‐transient VO2 kinetics in moderate or heavy exercise. VCO2 kinetics were slowed by a reduction in CO2 stores reflected in pre‐exercise and exercise end‐tidal CO2 pressure (PET,CO2) and plasma PCO2 which, we propose, contributed to slowed VE kinetics.