bluuebunny/crossref_metadata_2025_split huggingface dataset:
Drug Enforcement and Crime: Recent Evidence from New York State*
Authors: Shepard Edward M. , Blackley Paul R. 
Published: April 2005

Objective. The objective of this article is to provide evidence about the effectiveness of drug law enforcement as a tool for reducing other types of crime. Considerable resources are devoted to enforcing our nation's drug laws, but existing research suggests that intensifying drug law enforcement may serve to increase, rather than decrease, crime.Method. Using data for 62 counties in New York State for 1996–2000, we estimate a set of models that evaluate the effects of recent drug arrests on reported rates of assault, robbery, burglary, and larceny. The estimated statistical model includes controls for fixed effects, time effects, autocorrelation, and heteroskedasticity.Results. The consistency of results is striking—there is no model in which drug arrests are found to have a significant negative relationship with crime. All crimes are positively related to arrests for the manufacture and sale of “hard drugs.” Increases in total per capita drug arrests and arrests for “hard drug” possession are accompanied by higher rates for all crimes except assault. Increased arrests for the manufacture or sale of marijuana are associated with increases in larcenies.Conclusions. The empirical findings raise serious questions about the effectiveness of drug enforcement as a crime‐control measure and suggest that significant social costs may arise from existing approaches to drug control.
Induction of myocardial connective tissue growth factor in pacing‐induced heart failure in pigs
Authors: Ahmed M. S. , von Lueder T. G. , Øie E. , Kjekshus H. , Attramadal H. 
Published: April 2005

AbstractAims:  Connective tissue growth factor (CTGF) is a secreted, heparin‐binding, and extracellular matrix associated protein shown to stimulate many of the cellular events underlying fibrosis. Previous investigations have revealed that myocardial CTGF is substantially induced in ischaemic heart failure, particularly in the ischaemic and peri‐ischaemic region. The purpose of the present study was to investigate to what extent myocardial induction of CTGF is a general response to congestive heart failure (CHF) and to what extent CTGF is a decisive effector of fibrosis.Methods:  Experimental heart failure in pigs was induced by rapid pacing at 220–240 beats min−1 for 3 weeks (CHF pigs; n = 12).Results:  The CHF pigs exhibited significant left ventricular (LV) dilatation, reduced contractility, and increased cardiac filling pressures. Northern blot analysis demonstrated that myocardial CTGF mRNA levels in CHF pigs were fivefold higher (P < 0.05) than those in control pigs (n = 10). Similar elevations of immunoreactive CTGF (sixfold; P < 0.05) were observed in myocardial tissue samples prepared for Western blot analysis. Immunohistochemical analysis of myocardial tissue sections revealed predominant expression in interstitial and perivascular fibroblasts and endothelial cells. Myocardial procollagen α1(I) mRNA levels were also significantly elevated (sixfold; P < 0.05) in CHF pigs compared with controls, whereas myocardial tissue contents of collagen were not statistically different between the groups.Conclusion:  Induction of myocardial CTGF in heart failure is not just a response to ischaemia, but rather a general response to evolving heart failure. Yet, induction of myocardial CTGF was clearly not a sufficient effector of fibrosis.
The mitotic clock in skeletal muscle regeneration, disease and cell mediated gene therapy
Authors: Mouly V. , Aamiri A. , Bigot A. , Cooper R. N. , Di Donna S. , Furling D. , Gidaro T. , Jacquemin V. , Mamchaoui K. , Negroni E. , Périé S. , Renault V. , Silva‐Barbosa S. D. , Butler‐Browne G. S. 
Published: April 2005

AbstractThe regenerative capacity of skeletal muscle will depend on the number of available satellite cells and their proliferative capacity. We have measured both parameters in ageing, and have shown that although the proliferative capacity of satellite cells is decreasing during muscle growth, it then stabilizes in the adult, whereas the number of satellite cells decreases during ageing. We have also developed a model to evaluate the regenerative capacity of human satellite cells by implantation into regenerating muscles of immunodeficient mice. Using telomere measurements, we have shown that the proliferative capacity of satellite cells is dramatically decreased in muscle dystrophies, thus hampering the possibilities of autologous cell therapy. Immortalization by telomerase was unsuccessful, and we currently investigate the factors involved in cell cycle exits in human myoblasts. We have also observed that insulin‐like growth factor‐1 (IGF‐1), a factor known to provoke hypertrophy, does not increase the proliferative potential of satellite cells, which suggests that hypertrophy is provoked by increasing the number of satellite cells engaged in differentiation, thus possibly decreasing the compartment of reserve cells. We conclude that autologous cell therapy can be applied to specific targets when there is a source of satellite cells which is not yet exhausted. This is the case of Oculo–Pharyngeal Muscular Dystrophy (OPMD), a late onset muscular dystrophy, and we participate to a clinical trial using autologous satellite cells isolated from muscles spared by the disease.
Abnormal renal structural alterations during the development of diabetes mellitus in Otsuka Long‐Evans Tokushima Fatty rats*
Authors: Koike T. , Tomoda F. , Kinuno H. , Inoue H. , Takata M. 
Published: April 2005

AbstractAim:  The aim of this study was to investigate the renal structural properties in diabetic nephropathy.Methods:  Flow‐pressure and pressure‐glomerular filtration rate (GFR) relationships were determined for maximally vasodilated kidneys at 10 (pre‐diabetic stage) and 42 weeks of age (diabetic stage) in Otsuka Long‐Evans Tokushima Fatty rats (OLETF), an animal model of type 2 diabetes mellitus, using age‐matched Long‐Evans Tokushima Otsuka rats (LETO) as non‐diabetic controls (n = 9 of each age for each strain). Kidneys were then perfusion‐fixed for histological analysis.Results:  At 10 weeks of age, the slope of flow–pressure relationship (minimal renal vascular resistance, reflecting overall luminal dimensions of preglomerular and postglomerular vasculature) was steeper in OLETF than in LETO. In contrast, the threshold pressure for beginning filtration (preglomerular‐to‐postglomerular vascular resistance ratio) at pressure–GFR relationship did not differ between the two strains; however, the slope of the relationship (glomerular filtration capacity) was lower in OLETF than in LETO. Thus, in the kidneys of 10‐week‐old OLETF rats, vascular narrowing and impaired glomerular filtration capacity already existed with no abnormalities in preglomerular‐to‐postglomerular vascular resistance ratio. From the age of 10–42 weeks, the following results were obtained: (1) Minimal renal vascular resistance decreased in both strains, but it diminished markedly in OLETF. (2) The pressure for beginning filtration increased in LETO, but remained unchanged in OLETF. (3) Glomerular filtration capacity decreased to the similar extent in both strains. (4) Histologically, the vascular lumen and wall thickness increased in the interlobular arteries of both strains. However, vascular luminal widening was more pronounced in OLETF, resulting in the reduction in wall to lumen ratio. (5) Glomerular injuries and increased blood pressure occurred only in OLETF.Conclusion:  In conclusion, during progression from the prediabetic to diabetic stage of OLETF, the pre‐existing vascular narrowing was markedly attenuated without the concomitant increase in preglomerular‐to‐postglomerular vascular resistance ratio. Combined with increased blood pressure, these renal structural alterations could lead to the elevation of intraglomerular pressure in OLETF.
Effects of high‐intensity intermittent swimming on PGC‐1α protein expression in rat skeletal muscle
Authors: Terada S. , Kawanaka K. , Goto M. , Shimokawa T. , Tabata I. 
Published: April 2005

AbstractAim:  The aim of the present investigation was to elucidate the effects of exercise intensity on exercise‐induced expression of peroxisome proliferator‐activated receptor γ coactivator‐1α (PGC‐1α) protein in rat skeletal muscle.Methods:  We measured PGC‐1α content in the skeletal muscles of male Sprague–Dawley rats (age: 5–6 weeks old; body weight: 150–170 g) after a single session of high‐intensity intermittent exercise (HIE) or low‐intensity prolonged swimming exercise (LIE). During HIE, the rats swam for fourteen 20‐s periods carrying a weight (14% of body weight), and the periods of swimming were separated by a 10‐s pause. LIE rats swam with no load for 6 h in two 3‐h sessions, separated by 45 min of rest.Results:  After HIE, the PGC‐1α protein content in rat epitrochlearis muscle had increased by 126, 140 and 126% at 2, 6 and 18 h, respectively, compared with that of the age‐matched sedentary control rats’ muscle. Immediately, 6 and 18‐h after LIE, the PGC‐1α protein content in the muscle was significantly elevated by 84, 95 and 67% respectively. The PGC‐1α protein content observed 6 h after HIE tended to be higher than that observed after LIE. However, there was no statistically significant difference between the two values (P = 0.12).Conclusion:  The present investigation suggests that irrespective of the intensity of the exercise, PGC‐1α protein content in rat skeletal muscle increases to a comparable level when stimuli induced by different protocols are saturated. Further, HIE is a potent stimulus for enhancing the expression of PGC‐1αprotein, which may induce mitochondrial biogenesis in exercise‐activated skeletal muscle.
HSP20 phosphorylation and interstitial metabolites in hypoxia‐induced dilation of swine coronary arteries
Authors: Frøbert O. , Buus C. L. , Rembold C. M. 
Published: April 2005

AbstractObjective:  Hypoxia induces coronary artery dilation, but the responsible mechanism is largely unknown. Many stimuli induce arterial smooth muscle relaxation by reducing ser19‐myosin regulatory light chain (MLC) phosphorylation. Other stimuli can induce smooth muscle relaxation without reductions in ser19‐MLC phosphorylation. This form of relaxation has been termed force suppression and appears to be associated with heat shock protein 20 (HSP20) phosphorylation on ser16. We investigated whether hypoxia‐induced sustained dilation in swine coronary arteries was promoted without ser19‐MLC dephosphorylation and associated with ser16‐HSP20 phosphorylation. Nitroglycerin vasodilation served as control.Methods:  In a pressure myograph, the tunica media of intact pre‐contracted (PGF2α; 10−5 m) porcine coronary artery segments were cannulated using a microdialysis catheter. Diameter responses and interstitial lactate/pyruvate ratios were studied during 90 min hypoxia, hypoxia + reoxygenation (60 min), nitroglycerin (100 μm, 90 min), and nitroglycerin + wash‐out (60 min). The arterial segments were snap‐frozen and analysed for ser16‐HSP20 phosphorylation and ser19‐MLC phosphorylation.Results:  The normalized diameter responses to hypoxia (6.1 ± 4.3%) and nitroglycerin (12.6 ± 1.6%) were both significantly greater than normoxic control arteries (−10.5 ± 1.8%, anova, P < 0.05). Ser16‐HSP20 phosphorylation was increased with hypoxia and nitroglycerin treatment and ser16‐HSP20 phosphorylation correlated with changes in diameters (n = 29, r2 = 0.64, P < 0.001). Ser19‐MLC phosphorylation was not significantly altered by hypoxia. The lactate/pyruvate ratio was significantly increased in hypoxic arteries but did not correlate with diameters or ser16‐HSP20 phosphorylation.Conclusion:  Ser16‐HSP20 phosphorylation is a potential regulator of hypoxia‐induced dilation in coronary arteries.
Defective excitation‐contraction coupling in hearts of rats with congestive heart failure
Authors: Sjaastad I. , Birkeland J. A. , Ferrier G. , Howlett S. , Skomedal T. , Bjørnerheim R. , Wasserstrom J. A. , Sejersted O. M. 
Published: April 2005

AbstractAim:  We examined the cellular basis for depressed cardiac contractility in rats with congestive heart failure (CHF) secondary to myocardial infarction.Methods:  Six weeks after ligation of the left coronary artery, CHF was confirmed by haemodynamic measures and echocardiographic demonstration of reduced myocardial contractility in vivo. Papillary muscles from CHF animals developed less force than those from sham operated (SHAM) animals. Cell shortening was measured in isolated ventricular myocytes voltage‐clamped with high resistance electrodes. Ca2+ transients were measured in fluo‐4 loaded myocytes.Results:  Contractions triggered by depolarizing test steps from a post conditioning potential of −70 mV were significantly smaller and had significantly reduced velocity of shortening in CHF compared with SHAM myocytes. However, contractions initiated from −40 mV, were similar in amplitude and velocity of shortening in CHF and SHAM cells. L‐type Ca2+ current was not significantly different between CHF and SHAM cells, whether activated from −70 or −40 mV. Therefore, in SHAM cells, excitation‐contraction coupling exhibited higher gain when contractions were initiated from negative (−70 mV), as compared with depolarized potentials (−40 mV). However, in CHF myocytes, excitation‐contraction coupling gain was selectively depressed with steps from −70 mV. This depression of gain in CHF was not accompanied by a significant reduction in sarcoplasmic reticulum Ca2+ content. Isoproterenol increased Ca2+ transients less in CHF than SHAM myocytes.Conclusion:  In this post‐infarction model of CHF, the contractile deficit was voltage dependent and the gain of excitation‐contraction coupling was selectively depressed for contractions initiated negative to −40 mV.
Why do complications of gastrointestinal disease and procedures come as serial rather than singular events?
Authors: Sonnenberg A. 
Published: April 2005

AbstractBackground : It often appears as if complications arising from gastrointestinal disease and interventional procedures come in ‘series’ and ‘cluster’ in individual patients.Aim : The aim of this study was to analyse the clustering of complications in terms of stochastic modelling and Markov chains.Methods : A patient with gastrointestinal disease is simulated to move along either a ‘bad track’ associated with multiple consecutive complications or a ‘good track’ free of complications, the transitions within each track and between the two tracks being governed by probability values.Results : Because the occurrence of a single complication increases the risk of further complications, subjects who encounter their first complication are more likely to experience a second, third or even more complications, before they leave the ‘bad track’ and their personal chain of cascading complications becomes discontinued. The model of a Markov chain explains why the overall number of complications in the total population of patients with digestive disease remains low even if individual patients are expected to encounter more than a single complication.Conclusions : Published complication rates for gastrointestinal procedures underestimate the true risk to the patient, because they do not consider the added vulnerability to cascading complications after the first event.
Effect of different organic acids (citric, malic and ascorbic) on intragastric urease activity
Authors: Agha A. , Opekun A. R. , Abudayyeh S. , Graham D. Y. 
Published: April 2005

SummaryBackground: The mechanism of citric acid‐enhancedHelicobacter pyloriurease activity remains unclear.Aim: To compare ascorbic, citric and malic acid given at the same concentration and pH on intragastric urease activity.Methods: Volunteers received 40 mg of famotidine the evening prior to breath testing. After an overnight fast volunteers were randomized to receive 100 mL of water or 100 mmcitric, malic, or ascorbic acid, pH 2.3 containing 75 mg of13C‐urea. At 15 min a second 100 mL solution of one of the test solutions was taken without added urea.Results: Twelve volunteers were studied (eight men, four women, age 19–57, median 50.7) in a randomized‐crossover study. The mean breath test result at 30 min with ascorbic (17.5 ± 5), malic (25.8 ± 5) and citric acid (29.5 ± 5) were all significantly greater than with water (9.5 ± 3). Citric and malic acid were similar (P = 0.699) and significantly greater than ascorbic acid (P < 0.02). When the ascorbic acid was followed by citric acid, the result was similar to that with citrate alone (25.8 ± 4) and greater than with ascorbic then ascorbic (P = 0.026).Conclusions: Enhancement ofH. pyloriurease activity is not strictly a function of the pH. We propose the effect is related to differential effects of the availability of nickel, which is required for urease activity. Citric acid and malic acid were essentially equivalent such that malic acid could substitute for citric acid in the UBT; ascorbic acid would be a poor choice.
Multicentre randomized‐controlled clinical trial of Ipocol, a new enteric‐coated form of mesalazine, in comparison with Asacol in the treatment of ulcerative colitis
Authors: Forbes A. , Al‐Damluji A. , Ashworth S. , Bramble M. , Herbert K. , Ho J. , Kang J.‐Y. , Przemioslo R. , Shetty A. 
Published: April 2005

AbstractBackground : 5‐Aminosalicylates remain important in the treatment of ulcerative colitis, but it is uncertain if the various preparations currently available are equivalent given the different delivery systems that exist. Generic prescription of mesalazine (mesalamine) is therefore inappropriate. Ipocol has recently become available as an alternative to Asacol‐MR.Aim : To compare the two agents in a controlled trial using a non‐inferiority design.Methods : Eighty‐eight ulcerative colitis patients with a mild to moderate clinical relapse were randomized to one of the two drugs at a daily dose of 2.4 g for 8 weeks. Safety was the key concern; the primary measured end‐point was efficacy as judged from a colitis activity index.Results : There were no unexpected adverse events of clinical consequence. The colitis score improved similarly in both patient groups (by 2.3 with Ipocol and by 1.5 with Asacol: not significant), and a similar proportion was in clinical remission at the end of the study (26.1% for Ipocol and 28.6% for Asacol: not significant). Systemic steroids were needed in 11.9% of the Asacol‐treated patients compared with 6.5% with Ipocol (not significant).Conclusion : It appears appropriate to conclude that, while not identical to Asacol‐MR, Ipocol offers a safe and similarly effective alternative.
Inflammatory gene signature in ulcerative colitis with cDNA macroarray analysis
Authors: Okahara S. , Arimura Y. , Yabana T. , Kobayashi K. , Gotoh A. , Motoya S. , Imamura A. , Endo T. , Imai K. 
Published: April 2005

SummaryBackground : Most array analyses of ulcerative colitis have focused on identifying susceptibility genes for ulcerative colitis.Aim : To clarify the changes in gene expression during inflammation in ulcerative colitis colon mucosa using cDNA macroarray.Methods : From 23 ulcerative colitis patients, 16 each of inflamed and non‐inflamed specimens (total 32 samples for individual analysis) were obtained by colonoscopic biopsy. Eighteen of the 32 samples, used for pairwise analysis, consisted of nine sample pairs, each pair being from the same patient. We examined expression profiles of approximately 1300 genes with cDNA macroarray. Comparisons were made using two kinds of statistics, t‐test and significance analysis of microarray in both analyses. The reproducibility of significant genes from the macroarray analysis was confirmed by real‐time ploymerase chain reaction.Results : We detected five upregulated genes, categorized into proinflammatory genes (MRP14, GROγ and SAA1) and anti‐inflammatory genes (TIMP1 and Elafin) in inflamed mucosa, and one upregulated gene (L‐FABP) in non‐inflamed mucosa.Conclusions : As the cDNA macroarray analysis in this study exactly reflects the total profile of gene expression in the clinical setting of ulcerative colitis, the genes identified will be directly applicable to diagnostics or as novel therapeutic targets in active ulcerative colitis.
Managing dyspepsia without alarm signs in primary care: new national guidance for England and Wales
Authors: Mason J. M. , Delaney B. , Moayyedi P. , Thomas M. , Walt R. ,   The North of England Dyspepsia Guideline Development Group
Published: April 2005

AbstractAim : To report new recommendations for the primary care management of dyspepsia without alarm signs in England and Wales.Method : An independent, representative group of health care professionals, patient representatives and researchers developed the guideline using evidence‐based and small group‐working principles, and incorporated extensive peer‐reviewing and feedback from stakeholder organizations.Results : Referral to investigate dyspepsia should be made for alarm signs and not on the basis of age alone, reflecting the balance of benefit and harm from endoscopy. Empirical management without formal diagnosis is appropriate for most patients: reviewing patient history, lifestyle, over‐the‐counter medicines, and providing a course of proton‐pump inhibitors and/or Helicobacter pylori test and treatment. Patients with ongoing symptoms require at least annual review to discuss symptoms and lifestyle, and as appropriate, encourage stepping down prescribed medication and returning to self‐care. A new strategy included in the step down process is the use of therapies ‘on‐demand’.Conclusion : The guideline provides structured and supported recommendations for both undiagnosed and endoscopically investigated dyspepsia. Some favour increased investigation to detect Barrett's oesophagus and carcinoma. However, there is inconclusive evidence that patients without alarm signs will benefit subsequently from endoscopy, while investigation involves a small but real risk of harm.
Symptoms of gastro‐oesophageal reflux disease and the severity of obstructive sleep apnoea syndrome are not related in sleep disorders center patients
Authors: Kim H.‐N. , Vorona R. D. , Winn M. P. , Doviak M. , Johnson D. A. , Catesby Ware J. 
Published: April 2005

SummaryBackground : Studies suggest obstructive sleep apnea syndrome (OSAS) frequently manifests in patients with gastroesophageal reflux disease (GERD) and that there may be a causal relationship.Aim : To determine the relationship between OSAS and symptoms of GERD.Methods : Consecutive patients referred to the Sleep Disorders Center (SDC) 18 years and older with polysomnographically defined OSAS were evaluated prospectively for GERD using a validated symptoms questionnaire. The GERD and OSAS relationship was assessed by 1) determining frequency of GERD in patients with and without OSAS; 2) ascertaining the relationship between OSAS severity categories and presence of GERD; 3) examining GERD score in relation to those factors that might affect both GERD and OSAS, e.g. obesity.Results : One thousand and twenty‐three SDC patients met entry citeria. Amongst participants, GERD was common (29% of women and 17% of males) and OSAS extremely common (58% of women and 80% of males). GERD score did not correlate with OSAS variables. The severity of OSAS did not influence the prevalence of GERD.Conclusion : In a large group of patients referred to a sleep disorders center, there was no relationship between OSAS and GERD symptoms. Also, there was no relationship between the severity of OSAS and the likelihood of GERD symptoms.