bluuebunny/crossref_metadata_2025_split huggingface dataset:
The Isolation of Ricinoleic Acid from Castor Oil by Salt‐solubility‐based Fractionation for the Biopharmaceutical Applications
Authors: Vaisman Boris , Shikanov Ariella , Domb Abraham J. 
Published: December 2007

AbstractThe goal of this work was to develop a method for the preparative isolation of ricinoleic acid (RA) from Castor oil (CO) for use as building blocks in biopharmaceutical synthesis. The separation efficiency achieved with the impurity extraction approach (IEA) and the salting‐out approach (SOA) based on utilization of monobasic alkali salt of RA was examined. SOA showed better separation efficiency. Fractional precipitation from the co‐solvent system consisting of isopropyl ether:ethanol (IPE:EtOH) 65:35 v/v and applied at a CO: co‐solvent system mass: volume ratio of 1:5 produced a high quality purified RA (purity 97.9–98.6%). It contains residuals of linoleic acid and oleic acid as the main impurities and satisfies all requirements of the official compendia for oleaginous vehicles for parenteral administration. The total yield of this process was 55.5 ± 2.5% and the recovery of RA was about 70% (calculated relatively to the yield of the crude product). The study of the synthesis kinetics of RA oligomers and of the biopolymer prepared from these oligomers indicated that mono‐functional fatty acids (FAs) affect the composition of the oligomers' mixture and delay chain elongation of both RA oligomers and biopolymer. The developed novel process is simple, flexible, highly reproducible, inexpensive, and has high scalability potential.
The prevalence of personality disorder in schizophrenia and psychotic disorders: systematic review of rates and explanatory modelling
Authors: Newton-Howes G. , Tyrer P. , North B. , Yang M. 
Published: December 2007

BackgroundPersonality disorder (PD) in psychosis is poorly studied. As PD can affect outcome in mental disorders, it is important to understand its prevalence in order to plan services, understand prognosis more fully and maximize management options.MethodLiterature searching revealed 3972 potential papers. Twenty papers including 6345 patients were included in the final analysis. There was great variation in prevalence and multilevel modelling was used to identify possible reasons for this heterogeneity.ResultsThe prevalence of PD varied from 4.5% to 100%. Multilevel analysis suggested country of study, study type, the instruments used to diagnose PD and patient care correlated with the prevalence data explaining the study level heterogeneity, with 34.2, 33.4, 17.0 and 4.5% by each variable respectively. Personality studies in Canada and Sweden reported lower PD prevalence, whereas in Spain it was higher than the multinational study. Compared with randomized controlled trials, case-control studies reported lower prevalence [odds ratio (OR)=0.35, 95% confidence interval (CI) 0.15–0.79] and observational studies higher prevalence (OR 70.5, 95% CI 8.5–583). Primary-care patients were less likely to be diagnosed (OR 0.02, 95% CI 0–0.19) than hospital patients, and out-patients had higher prevalence (OR 12.5, 95% CI 1.77–88.6).ConclusionsThe reported prevalence of PD in schizophrenia varies significantly. Statistical modelling suggests care, country, study type and diagnostic tools for PD all bias prevalence rates. The number of papers reaching the inclusion criteria, the relative paucity of information and the difficulties in developing an accurate statistical model limited interpretation from the study.
Toward an understanding of risk factors for anorexia nervosa: a case-control study
Authors: Pike K. M. , Hilbert A. , Wilfley D. E. , Fairburn C. G. , Dohm F.-A. , Walsh B. T. , Striegel-Moore R. 
Published: December 2007

BackgroundProspective, longitudinal studies of risk factors for anorexia nervosa (AN) are lacking and existing cross-sectional studies are generally narrow in focus and lack methodological rigor. Building on two studies that used the Oxford Risk Factor Interview (RFI) to establish time precedence and comprehensively assess potential risk correlates for AN, the present study advances this line of research and represents the first case-control study of risk factors for AN in the USA.MethodThe RFI was used for retrospective assessment of a broad range of risk factors, while establishing time precedence. Using a case-control design, 50 women who met DSM-IV criteria for AN were compared to those with non-eating disorder DSM-IV psychiatric disorders (n=50) and those with no psychiatric disorder (n=50).ResultsWomen with psychiatric disorders reported higher rates of negative affectivity, maternal and paternal parenting problems, family discord, parental mood and substance disorder, and physical and sexual abuse than women with no psychiatric disorder. Women with AN specifically reported greater severity and significantly higher rates of negative affectivity, perfectionism and family discord, and higher parental demands than women with other psychiatric disorders. The role of weight and shape concerns was most salient in the year preceding onset of AN.ConclusionsConvergent data identifying common risk factors as well as those more severe in the development of AN are emerging to inform longitudinal risk factor and prevention studies for this disorder.
Snus use and other correlates of smoking cessation in the Swedish Twin Registry
Authors: Furberg H. , Lichtenstein P. , Pedersen N. L. , Bulik C. M. , Lerman C. , Sullivan P. F. 
Published: December 2007

BackgroundWe investigated 12 variables and their interactions as correlates of smoking cessation among regular smokers in the population-based Swedish Twin Registry (STR).MethodDetailed information on tobacco use and personal characteristics were available from 14 715 male and female twins aged 42–64 years who participated in a screening of the population-based STR and reported being regular smokers in their lifetime. A two-stage analytic design was used to examine correlates of smoking cessation. The sample was split at random and significant main effects and interactions identified in the testing set were examined in the validation set. Hazard ratios (HRs) and 95% confidence intervals (CIs) describe the association between correlates and smoking cessation.ResultsTwelve main effects were significantly associated with smoking cessation in the testing set; eight were confirmed in the validation set. Of the nine interactions identified in the testing set, none remained significant when evaluated in the validation set after Bonferroni correction. HRs were highest for Swedish oral smokeless tobacco (snus) use (HR 2.70, 95% CI 2.30–3.20), >11 years of education (HR 1.57, 95% CI 1.43–1.73) and being married or cohabitating (HR 1.51, 95% CI 1.39–1.63). Although not statistically significant after Bonferroni correction, snus use also appeared important in the context of interactions, where lower nicotine dependence score, higher socio-economic status (SES) and greater body size were associated with smoking cessation only among participants who never used snus.ConclusionsSnus use was the strongest independent correlate of smoking cessation. Further studies should investigate the mechanism of this association.
Associations between ethnicity and self-reported hallucinations in a population sample of young adults in The Netherlands
Authors: Vanheusden K. , Mulder C. L. , van der Ende J. , Selten J.-P. , van Lenthe F. J. , Verhulst F. C. , Mackenbach J. P. 
Published: December 2007

BackgroundPsychotic disorders are more common in people from ethnic minorities. If psychosis exists as a continuous phenotype, ethnic disparities in psychotic disorder will be accompanied by similar ethnic disparities in the rate of psychotic symptoms. This study examined ethnic disparities in self-reported hallucinations in a population sample of young adults.MethodA cross-sectional population survey (n=2258) was carried out in the south-west Netherlands. Seven ethnic groups were delineated: Dutch natives, Turks, Moroccans, Surinamese/Antilleans, Indonesians, other non-Western immigrants (mostly from Africa or Asia) and Western immigrants (mostly from Western Europe). Self-reported auditory and visual hallucinations were assessed with the Adult Self-Report (ASR). Indicators of social adversity included social difficulties and a significant drop in financial resources.ResultsCompared to Dutch natives, Turkish females [odds ratio (OR) 13.48, 95% confidence interval (CI) 5.97–30.42], Moroccan males (OR 8.36, 95% CI 3.29–21.22), Surinamese/Antilleans (OR 2.19, 95% CI 1.05–4.58), Indonesians (OR 4.15, 95% CI 1.69–10.19) and other non-Western immigrants (OR 3.57, 95% CI 1.62–7.85) were more likely to report hallucinations, whereas Western immigrants, Turkish males and Moroccan females did not differ from their Dutch counterparts. When adjusting for social adversity, the ORs for self-reported hallucinations among the non-Western immigrant groups showed considerable reductions of 28% to 52%.ConclusionsIn a general population sample, several non-Western immigrant groups reported hallucinations more often than Dutch natives, which is consistent with the higher incidence of psychotic disorders in most of these groups. The associations between ethnicity and hallucinations diminished after adjustment for social adversity, which supports the view that adverse social experiences contribute to the higher rate of psychosis among migrants.
TILL DEATH DO US PART
Authors: Diel Lori Boornazian 
Published: December 2007

AbstractThough infrequent, the inclusion of marriage statements in Aztec histories reveals the political nature of matrimony for elite Nahua rulers in Late Postclassic-period central Mexico. The rules governing these elite marriages were so standardized that unconventional marriages particularly stand out as strong political declarations. This article focuses on four case studies—two marriages that violated already established political alliances and two marriages in which aggressions were taken out against the royal wives. These case studies reveal shifting alliances and political maneuvering that are not as clearly evident when looking strictly at Conquest history. Ultimately, these marriages illuminate increasing political tensions within the Aztec empire. Moreover, they reveal the potential, though largely hidden, role of noblewomen in Aztec politics. Clearly, the political stakes in these unconventional marriages were high; in the four cases studies presented here, each ends with the death of one of the spouses.
DROUGHT AND THE MAYA COLLAPSE
Authors: Gill Richardson B. , Mayewski Paul A. , Nyberg Johan , Haug Gerald H. , Peterson Larry C. 
Published: December 2007

AbstractBetween a.d. 760 and 930, millions of Maya disappeared from the Earth. We examine changes in the physical environment in which the Maya lived. The ice-core evidence from Greenland indicates that around the time of the Maya Collapse, a minimum in solar insolation and a low in solar activity occurred, accompanied by severe cold and dryness over Greenland, indicating hemispheric climatic conditions propitious for drought in the Maya Lowlands. In the northeastern Caribbean, sea-surface salinity (SSS) was lowered. The most severe drought of the past 7,000 years devastated the Yucatan Peninsula. Large Maya cities collapsed in four phases of abandonment spaced about fifty years apart around a.d. 760, 810, 860, and 910. A new core taken from Lake Chichancanab in Quintana Roo shows three peak episodes of brutal drought within a 150- to 200-year drought. A marine core from the Cariaco Basin off Venezuela precisely dates four severe drought episodes to 760, 810, 860, and 910, coincident with the four phases of abandonment of cities. The long-term drought appears to have lasted from 760 to 930 in the Cariaco Basin. The climatic changes were the most drastic the Maya had faced in the preceding 1,500 years and the most severe of the preceding 7,000 years.
The cardiac persistent sodium current: an appealing therapeutic target?
Authors: Saint D A 
Published: December 2007

The sodium current in the heart is not a single current with a mono‐exponential decay but rather a mixture of currents with different kinetics. It is not clear whether these arise from distinct populations of channels, or from modulation of a single population. A very slowly inactivating component, [INa(P)] INa(P)is usually about 1% of the size of the peak transient current [INa(T)], but is enhanced by hypoxia. It contributes to Na+loading and cellular damage in ischaemia and re‐perfusion, and perhaps to ischaemic arrhythmias. Class I antiarrhythmic agents such as flecainide, lidocaine and mexiletine generally block INA(P)more potently than block of INa(T)and have been used clinically to treat LQT3 syndrome, which arises because mutations in SCN5A produce defective inactivation of the cardiac sodium channel. The same approach may be useful in some pathological situations, such as ischaemic arrhythmias or diastolic dysfunction, and newer agents are being developed with this goal. For example, ranolazine blocks INa(P)about 10 times more potently than INa(T)and has shown promise in the treatment of angina. Alternatively, the combination of INa(P)block with K+channel block may provide protection from the induction of Torsades de Pointe when these agents are used to treat atrial arrhythmias (eg Vernakalant). In all of these scenarios, an understanding of the role of INa(P)in cardiac pathophysiology, the mechanisms by which it may affect cardiac electrophysiology and the potential side effects of blocking INa(P)in the heart and elsewhere will become increasingly important.British Journal of Pharmacology(2008)153, 1133–1142; doi:10.1038/sj.bjp.0707492; published online 10 December 2007
Inhibition of late sodium current to reduce electrical and mechanical dysfunction of ischaemic myocardium
Authors: Shryock J C , Belardinelli L 
Published: December 2007

This commentary on the review by DA Saint in the current issue of the British Journal of Pharmacology focuses on the pathological role of late INa in the heart, the evidence supporting inhibition of late INa as a therapeutic target in ischaemic heart disease, and the therapeutic applications and challenges for development of new late INa inhibitors. Recent reports from a large clinical outcome trial (MERLIN) of ranolazine, a drug known to inhibit late INa, indicated that it was safe and reduced recurrent ischaemia and arrhythmic activity. In combination with other results indicating that inhibition of late INa reduces ischaemia, myocardial Ca2+ overload, and electrical and mechanical dysfunction when late INa is increased, the new clinical trial results suggest that reduction of cardiac late INa is safe and therapeutically beneficial.British Journal of Pharmacology (2008) 153, 1128–1132; doi:10.1038/sj.bjp.0707522; published online 10 December 2007
Cannabinoid receptors and the regulation of bone mass
Authors: Bab I , Zimmer A 
Published: December 2007

A functional endocannabinoid system is present in several mammalian organs and tissues. Recently, endocannabinoids and their receptors have been reported in the skeleton. Osteoblasts, the bone forming cells, and osteoclasts, the bone resorbing cells, produce the endocannabinoids anandamide and 2‐arachidonoylglycerol and express CB2 cannabinoid receptors. Although CB2 has been implicated in pathological processes in the central nervous system and peripheral tissues, the skeleton appears as the main system physiologically regulated by CB2. CB2‐deficient mice show a markedly accelerated age‐related bone loss and theCNR2gene (encoding CB2) in women is associated with low bone mineral density. The activation of CB2 attenuates ovariectomy‐induced bone loss in mice by restraining bone resorption and enhancing bone formation. Hence synthetic CB2 ligands, which are stable and orally available, provide a basis for developing novel anti‐osteoporotic therapies. Activation of CB1 in sympathetic nerve terminals in bone inhibits norepinephrine release, thus balancing the tonic sympathetic restrain of bone formation. Low levels of CB1 were also reported in osteoclasts. CB1‐null mice display a skeletal phenotype that is dependent on the mouse strain, gender and specific mutation of the CB1 encoding gene,CNR1.British Journal of Pharmacology(2008)153, 182–188; doi:10.1038/sj.bjp.0707593; published online 10 December 2007
Role of the NO/cGMP/KATP pathway in the protective effects of sildenafil against ethanol‐induced gastric damage in rats
Authors: Medeiros J V R , Gadelha G G , Lima S J , Garcia J A , Soares P M G , Santos A A , Brito G A C , Ribeiro R A , Souza M H L P 
Published: December 2007

Background and purpose:Sildenafil is a selective inhibitor of cGMP‐specific phosphodiesterase. Sildenafil, acting via NO‐dependent mechanisms, prevents indomethacin‐induced gastropathy. Activation of ATP‐sensitive potassium channels (KATP) is involved in gastric defence. Our objective was to evaluate the role of the NO/cGMP/KATP pathway in the protective effects of sildenafil against ethanol‐induced gastric damage.Experimental approach:Rats were treated with L‐NAME (1 or 3 mg kg−1, i.p.) or with L‐arginine (200 mg kg−1, i.p.) +L‐NAME (3 mg kg−1, i.p.), the guanylate cyclase inhibitor, ODQ (10 mg kg−1, i.p.), glibenclamide (0.1, 0.3, 1 or 3 mg kg−1, i.p.) or with glibenclamide (1 mg kg−1, i.p.) + diazoxide (3 mg kg−1, i.p.). After thirty minutes, the rats received sildenafil (1 mg kg−1, by gavage), followed by intragastric instillation of absolute ethanol (4 ml kg−1) to induce gastric damage. One hour later, gastric damage (haemorrhagic or ulcerative lesions) was measured with a planimetry programme. Samples of stomach were also taken for histopathological assessment and for assays of tissue glutathione and haemoglobin.Key results:Sildenafil significantly reduced ethanol‐induced gastric damage in rats. L‐NAME alone, without L‐arginine, significantly reversed the protection afforded by sildenafil. Inhibition of guanylate cyclase by ODQ completely abolished the gastric protective effect of sildenafil against ethanol‐induced gastric damage. Glibenclamide alone reversed sildenafil's gastric protective effect. However, glibenclamide plus diazoxide did not alter the effects of sildenafil.Conclusions:Sildenafil had a protective effect against ethanol‐induced gastric damage through the activation of the NO/cGMP/KATP pathway. British Journal of Pharmacology (2008) 153, 721–727; doi:10.1038/sj.bjp.0707605; published online 10 December 2007
Rifampicin exacerbates isoniazid‐induced toxicity in human but not in rat hepatocytes in tissue‐like cultures
Authors: Shen C , Meng Q , Zhang G , Hu W 
Published: December 2007

Background and purpose:Rifampicin has been extensively reported to exacerbate the hepatotoxicity of isoniazid in patients with tuberculosis. However, this was controversially claimed by previous reports using rat models. This study evaluated the effect of rifampicin on isoniazid‐induced hepatocyte toxicity by using human and rat hepatocytes in tissue‐like culture.Experimental approach:Hepatocytes in tissue‐like gel entrapment were used to examine isoniazid toxicity, as shown by cell viability, intracellular glutathione content and albumin secretion. For demonstration of the differential effects of rifampicin on human and rat hepatocytes, induction by rifampicin of cytochromeP450 (CYP) 2E1, a major enzyme associated with isoniazid hepatotoxicity, was detected by 4‐nitrocatechol formation and RT‐PCR analysis.Key results:Rifampicin (12 μM) enhanced isoniazid‐induced toxicity in human hepatocytes but not in rat hepatocytes. Enhanced CYP 2E1 enzymic activity and mRNA expression were similarly detected in human hepatocytes but not in rat hepatocytes. Both rat and human hepatocytes in gel entrapment were more sensitive to isoniazid treatment compared with the corresponding hepatocytes in a monolayer culture.Conclusions and implications:The difference in induction of CYP 2E1 by rifampicin between rat and human hepatocytes accounted for the difference in exacerbation of isoniazid hepatocyte toxicity by rifampicin, with more significant toxicity in gel entrapment than in monolayer cultures. Thus, human hepatocytes in tissue‐like cultures (gel entrapment) could be an effective model for hepatotoxicity researchin vitro, closer to thein vivosituation.British Journal of Pharmacology(2008)153, 784–791; doi:10.1038/sj.bjp.0707611; published online 10 December 2007
α1‐Adrenoceptor antagonists prevent paracetamol‐induced hepatotoxicity in mice
Authors: Randle L E , Sathish J G , Kitteringham N R , Macdonald I , Williams D P , Park B K 
Published: December 2007

Background and purpose:Paracetamol, a major cause of acute liver failure (ALF) represents a significant clinical problem. Adrenoceptor stimulation or antagonism can modulate chemical‐induced hepatotoxicity. We investigated the role of endogenous catecholamines and α1‐adrenoceptors in the development of paracetamol‐ induced hepatotoxicity.Experimental approach:Paracetamol (3.5 mmol kg−1) was administered to male CD‐1 mice, with and without α1‐adrenoceptor antagonists (prazosin, doxazosin, terazosin and tamsulosin; 35.7 μmol kg−1). Serum transaminases and hepatic glutathione (GSH) levels were assessed as markers of hepatic damage. Paracetamol bioactivation was assessed by covalent binding, hepatic and urinary conjugate formation and uridine glucuronosyltransferase activity. Plasma catecholamines levels and hepatic congestion were also analysed.Key results:Plasma catecholamine levels were significantly elevated 5 h post paracetamol administration. Prazosin prevented hepatotoxicity when administered 1 h before a toxic paracetamol insult and importantly, when administered up to 1 h post paracetamol injection. Prazosin had no effect on paracetamol‐induced depletion of hepatic GSH, paracetamol bioactivation or paracetamol‐induced transcription of defence genes. Paracetamol toxicity is associated with marked accumulation of erythrocytes within hepatic sinusoids and prazosin completely prevented this accumulation.Conclusion and implications:Paracetamol‐induced hepatocellular damage is associated with increased circulating catecholamines. α1‐Adrenoceptor antagonists conferred complete protection from paracetamol ‐induced hepatotoxicity. Protection was associated with absence of hepatic erythrocyte accumulation. Increased catecholamine levels may contribute to the pathophysiology of paracetamol‐induced hepatotoxicity by compromising hepatic perfusion. Protection against paracetamol toxicity by α1antagonists in mice has implications for therapeutic management of patients presenting with paracetamol overdose and ALF.British Journal of Pharmacology(2008)153, 820–830; doi:10.1038/sj.bjp.0707620; published online 10 December 2007