bluuebunny/crossref_metadata_2025_split huggingface dataset:
Caffeine does not attenuate experimentally induced ischemic pain in healthy subjects
Authors: DELLERMALM J. , SEGERDAHL M. , GRASS S. 
Published: June 2009

Background and aims:Caffeine is likely the most widely used psychoactive substance in the world. It is also an analgesic adjuvant and has individual analgesic properties. The latter effect has been attributed to adenosine receptor antagonism, but the site of action is unknown. The aim of this study was to investigate the analgesic properties of caffeine on experimentally induced ischemic pain and to attempt to elucidate whether the site of action is central or peripheral.Materials and methods:Seventeen healthy subjects received intravenous (i.v.) regional and systemic infusions of caffeine at 10 mg/kg or placebo in a double‐blind, crossover fashion to investigate the site of action for caffeine‐induced analgesia. Subjects underwent a sub‐maximum effort tourniquet test. Pain scores [visual analogue scale (VAS), 0–100] were assessed every minute up to a maximum of 45 min.Results:The sum of pain scores (SPS, accumulation of VAS scores) was attenuated neither by systemic 2405 (±234) nor by i.v. regional caffeine 2427 (±190) as compared with placebo 2442 (±205),P=0.99 (mean±SEM). Time to maximal VAS score did not differ significantly between treatments,P=0.94. There was no correlation between caffeine concentration in plasma and time to maximal pain score, or between SPS and plasma concentration.Conclusion:Caffeine does not have an analgesic effect on ischemic pain, either by a peripheral or by a central site of action.
DNA methylation patterns at the IGF2‐H19 locus in sperm of Swiss Landrace and Swiss Large White boars
Authors: Giannini Petra , Braunschweig Martin 
Published: June 2009

SummaryDNA methylation patterns at the IGF2‐H19 locus were investigated in sperm DNA from Swiss Landrace (SL) and Swiss Large White (LW) boars. The putative IGF2 differentially methylated regions (DMR) 0, 1 and 2, a quantitative trait nucleotide (QTN) region in the intron 3 and a CpG island in the intron 4 of the IGF2 gene as well as three regions around porcine CTCF binding sites within the H19 differentially methylated domain (DMD) were selected for the DNA methylation analysis. In both breeds putative IGF2 DMR0, 1, 2 and H19 DMD were hypermethylated. Significant differences in DNA methylation content were found between the two breeds in the two DMD regions proximal to the H19 gene. The IGF2 QTN region and the CpG island in the IGF2 intron 4 were hypomethylated in sperm DNA of both breeds. The methylation analysis revealed significantly more methylated CpG sites in the intron 4 of sperm from the LW breed than in that from SL. No difference was found in global DNA methylation between the two breeds. These results indicate differences in DNA methylation patterns between breeds and it remains to be established whether variation in DNA methylation patterns impacts on phenotypic traits.
Novel SSR Markers for Polymorphism Detection in Pigeonpea (Cajanus spp.)
Authors: Saxena R. K. , Prathima C. , Saxena K.B. , Hoisington D. A. , Singh N. K. , Varshney R. K. 
Published: June 2009

With 1 figure and 4 tables AbstractWith an objective to expand the repertoire of molecular markers in pigeonpea (Cajanus cajan), 36 microsatellite or simple sequence repeat (SSR) loci were isolated from a SSR‐enriched genomic library. Primer pairs were designed for 23 SSR loci, of which 16 yielded amplicons of expected size. Thirteen SSR markers were polymorphic amongst 32 cultivated and eight wild pigeonpea genotypes representing six Cajanus species. These markers amplified a total of 72 alleles ranging from two to eight alleles with an average of 5.5 alleles per locus. The polymorphic information content for these markers ranged from 0.05 to 0.55 with an average of 0.32 per marker. Phenetic analysis clearly distinguished all wild species genotypes from each other and from the cultivated pigeonpea genotypes. These markers should be useful for genome mapping, trait mapping, diversity studies and assessment of gene flow between populations in pigeonpea.
Tribble 3, a novel oxidized low‐density lipoprotein‐inducible gene, is induced via the activating transcription factor 4–C/EBP homologous protein pathway
Authors: Shang Yuan‐Yuan , Zhong Ming , Zhang Li‐Ping , Guo Zhong‐Xiu , Wang Zhi‐Hao , Zhang Yun , Deng Jing‐Ti , Zhang Wei 
Published: June 2009

Summary1. C/EBP homologueueueous protein (CHOP), an endoplasmic reticulum (ER) stress‐inducible protein, has a critical role in regulation of the cell cycle and apoptosis by forming heterodimers with other C/EBP proteins. However, how CHOP function is regulated remains to be determined. The human homologue of Drosophila tribbles (TRIB3) is associated with CHOP and is upregulated by oxidized low‐density lipoprotein (ox‐LDL). The aim of the present study was to investigate the role of CHOP in ox‐LDL‐induced TRIB3 expression in macrophages.2. Human monocyte‐derived macrophages were treated with various concentrations of ox‐LDL (0, 2.5, 5, 10, 25 and 50 μg/mL) or 2 μg/mL tunicamycin for 0, 4, 8, 16, 24 and 48 h or were transfected with CHOP or TRIB3 expression plasmid and TRIB3 targeting short interference RNA (siRNA). The expression of CHOP and activating transcription factor 4 (ATF4) mRNA in treated cells was detected by quantitative real‐time polymerase chain reaction (PCR).3. The expression of CHOP and ATF4 mRNA increased with increasing concentrations of ox‐LDL and duration of time. The ox‐LDL‐induced expression of TRIB3 mRNA was upregulated later than the expression of CHOP and ATF4 mRNA. Overexpression of CHOP increased the mRNA expression of TRIB3, which was further increased in CHOP‐overexpressing macrophages treated with ox‐LDL. Overexpression of TRIB3 suppressed the expression of CHOP, whereas TRIB3 silencing increased CHOP expression following ox‐LDL stimulation by a negative feedback mechanism.4. In conculsion, the expression of ATF4 and CHOP is upregulated by ox‐LDL in a dose‐ and time‐dependent manner in naturally differentiated human macrophages. Oxidized LDL induces TRIB3 expression via an ATF4/CHOP‐dependent ER stress pathway.
New strategies for the prevention of stroke
Authors: Liu Ai‐Jun , Guo Jin‐Min , Xia Weiliang , Su Ding‐Feng 
Published: June 2009

Summary1. Stroke is a major cause of disability and death worldwide. It is preferable to prevent stroke rather than to treat it and, for the prevention of stroke, all risk factors relating to stroke need to be understood. The present paper reviews potential new strategies for the prevention of stroke based on findings of new risk factors, as well as classical risk factors.2. Recently, new risk factors related to stroke were reported, including dysfunction of the arterial baroreflex, pro‐inflammatory cytokines, vitamins and hormone deficiency. Correspondingly, therapies targeting these risk factors where shown to significantly reduce the incidence and/or severity of stroke.3. Because the genesis of stroke is multifactorial, the prevention of stroke should not target one risk factor only. Combination therapies with drugs acting on different risk factors may be more effective in the prevention of stroke.
Rosiglitazone‐induced myocardial protection against ischaemia–reperfusion injury is mediated via a phosphatidylinositol 3‐kinase/Akt‐dependent pathway
Authors: Zhang Xue‐Jiao , Xiong Zi‐Bo , Tang An‐Li , Ma Hong , Ma Yue‐Dong , Wu Jing‐Guo , Dong Yu‐Gang 
Published: June 2009

Summary1. Rosiglitazone is widely used in the treatment of Type 2 diabetes. However, in recent years it has become evident that the therapeutic effects of peroxisome proliferator‐activated receptor γ ligands reach far beyond their use as insulin sensitizers. Recently, the ability of rosiglitazone pretreatment to induce cardioprotection following ischaemia–reperfusion (I/R) has been well documented; however, the protective mechanisms have not been elucidated. In the present study, examined the role of the phosphatidylinositol 3‐kinase (PI3‐K)/Akt signalling pathway in rosiglitazone cardioprotection following I/R injury.2. Mice were pretreated with 3 mg/kg per day rosiglitazone for 14 days before hearts were subjected to ischaemia (30 min) and reperfusion (2 h). Wortmannin (1.4 mg/kg, i.p.), an inhibitor of PI3‐K, was administered 10 min prior to myocardial I/R. Then, activation of the PI3‐K/Akt/glycogen synthase kinase (GSK)‐3α signalling pathway was examined. The effects of PI3‐K inhibition on rosiglitazone‐induced cardioprotection were also evaluated.3. Compared with control rats, the ratio of infarct size to ischaemic area (area at risk) and the occurrence of sustained ventricular fibrillation in rosiglitazone‐pretreated rats was significantly reduced (P < 0.05). Rosiglitazone pretreatment attenuated cardiac apoptosis, as assessed by ELISA to determine cardiomyocyte DNA fragmentation. Rosiglitazone pretreatment significantly increased levels of phosphorylated (p‐) Akt and p‐GSK‐3α in the rat myocardium. Pharmacological inhibition of PI3‐K by wortmannin markedly abolished the cardioprotection induced by rosiglitazone.4. These results indicate that rosiglitazone‐induced cardioprotection in I/R injury is mediated via a PI3‐K/Akt/GSK‐3α‐dependent pathway. The data also suggest that modulation of PI3‐K/Akt/GSK‐3α‐dependent signalling pathways may be a viable strategy to reduce myocardial I/R injury.
Angiotensin II and neurohumoral control of the renal medullary circulation
Authors: Evans Roger G , Head Geoffrey A , Eppel Gabriela A , Burke Sandra L , Rajapakse Niwanthi W 
Published: June 2009

Summary1. Angiotensin (Ang) II has multiple actions in the renal medullary circulation. It can induce vasodilatation and blunt the response of medullary blood flow (MBF) to renal nerve activation through AT1receptor‐mediated release of nitric oxide (NO) and/or vasodilator prostaglandins. These actions require high intravascular and/or intratubular AngII concentrations, so are not apparent under physiological conditions.2. Nevertheless, these mechanisms blunt the responsiveness of MBF to AT1receptor‐mediated vasoconstriction. When these protective mechanisms fail, as when oxidative stress reduces NO bioavailability in the medullary circulation, AngII reduces MBF. If sustained, reduced MBF leads to the development of hypertension.3. Chronic activation of the renin–angiotensin system (RAS) induces oxidative stress in the kidney. Therefore, MBF may be reduced in models of hypertension associated with RAS activation both because AngII levelsper seare increased and because of increased responsiveness of MBF to AngII‐induced vasoconstriction.4. Endogenous AngII enhances the responsiveness of MBF to renal nerve stimulation, whereas NO blunts it. Chronic RAS activation and/or oxidative stress should therefore be expected to enhance MBF responses to renal nerve stimulation. Consistent with this, reductions in MBF induced by renal nerve stimulation are enhanced in rabbits with AngII‐induced hypertension, renovascular hypertension or after 9 weeks of fat feeding.5. We conclude that the ability of endogenous AngII to reduce MBF and enhance the response of MBF to activation of the renal nerves could contribute to the development of hypertension under conditions of RAS activation, especially if accompanied by increased renal sympathetic nerve activity.
Brain cytokines as neuromodulators in cardiovascular control
Authors: Shi Peng , Raizada Mohan K , Sumners Colin 
Published: June 2009

Summary1. The role of cytokines in cardiovascular control, especially in neurogenic hypertension, has received considerable attention during the past few years. Brain cytokines have been shown to exert profound effects on neuronal activity. Recently, a number of studies have shown that administration of pro‐inflammatory cytokines or anti‐inflammatory cytokines into the central nervous system has a significant impact on sympathetic outflow, arterial pressure and cardiac remodelling in experimental models of hypertension and heart failure.2. Our objective in this review is to present a succinct account of the effect of cytokines on neuronal activity and their role in cardiovascular disease. Furthermore, we propose a hypothesis for a neuromodulatory role of cytokines in the neural control of cardiovascular function.
Ghrelin gene‐related peptides: Multifunctional endocrine / autocrine modulators in health and disease
Authors: Seim Inge , Amorim Laura , Walpole Carina , Carter Shea , Chopin Lisa K , Herington Adrian C 
Published: June 2009

Summary1. Ghrelin is a multifunctional peptide hormone that affects various processes, including growth hormone and insulin release, appetite regulation, gut motility, metabolism and cancer cell proliferation. Ghrelin is produced in the stomach and in other normal and pathological cell types. It may act as an endocrine or autocrine/paracrine factor.2. The present article reviews recent findings in the study of ghrelin and its receptor that suggest that the ghrelin gene locus may give rise to a number of functional molecules (peptides and RNA transcripts) in addition to ghrelin.3. The ghrelin gene encodes a precursor protein, preproghrelin, from which ghrelin and other potentially active peptides are derived by alternative mRNA splicing and/or proteolytic processing. The metabolic role of the peptide obestatin, derived from the preproghrelin C‐terminal region, is contentious. However, obestatin has direct effects on cell proliferation.4. The regulation of ghrelin expression and the mechanisms through which the peptide products arise are unclear. We have recently re‐examined the organization of the ghrelin gene and identified several novel exons and transcripts. One transcript, which lacks the ghrelin‐coding region of preproghrelin, contains the coding sequence of obestatin.5. Furthermore, we have identified an overlapping gene on the antisense strand of ghrelin, namely GHRLOS, which generates transcripts that may function as non‐coding regulatory RNAs or code for novel, short bioactive peptides.6. The identification of these novel ghrelin‐gene related transcripts and peptides raises critical questions regarding their physiological function and their potential role in obesity, diabetes and cancer.
Multidrug resistance‐associated proteins and implications in drug development
Authors: Liu Ya‐He , Di Yuan‐Ming , Zhou Zhi‐Wei , Mo Sui‐Lin , Zhou Shu‐Feng 
Published: June 2009

Summary1. The multidrug resistance‐associated proteins (MRPs) belong to the ATP‐binding cassette superfamily (ABCC family) of transporters that are expressed differentially in the liver, kidney, intestine and blood–brain barrier. There are nine human MRPs that transport a structurally diverse array of endo‐ and xenobiotics as well as their conjugates.2. Multidrug resistance‐associated protein 1 can be distinguished from MRP2 and MRP3 by its higher affinity for leukotriene C4. Unlike MRP1, MRP2 functions in the extrusion of endogenous organic anions, such as bilirubin glucuronide and certain anticancer agents. In addition to the transport of glutathione and glucuronate conjugates, MRP3 has the additional capability of mediating the transport of monoanionic bile acids.3. Both MRP4 and MRP5 are able to mediate the transport of cyclic nucleotides and confer resistance to certain antiviral and anticancer nucleotide analogues. Hereditary deficiency of MRP6 results in pseudoxanthoma elasticum. In the body, MRP6 is involved in the transport of glutathione conjugates and the cyclic pentapeptide BQ123.4. Various MRPs show considerable differences in tissue distribution, substrate specificity and proposed physiological function. These proteins play a role in drug disposition and excretion and thus are implicated in drug toxicity and drug interactions. Increased efflux of natural product anticancer drugs and other anticancer agents mediated by MRPs from cancer cells is associated with tumour resistance.5. A better understanding of the function and regulating mechanisms of MRPs could help minimize and avoid drug toxicity and unfavourable drug–drug interactions, as well as help overcome drug resistance.
Supraventricular tachycardia as a presenting feature of volvulus in a 15‐month‐old boy
Authors: Jacombs Anita SW , Cross Kate M , Holland Andrew JA , Wilkins Barry H 
Published: June 2009

Abstract:A 15‐month‐old boy presented in shock with a supraventricular tachycardia following a 12‐h history of worsening abdominal pain and vomiting. The supraventricular tachycardia reverted to sinus tachycardia with fluid resuscitation and adenosine. He was noted to have a distended and firm abdomen. A presumptive diagnosis of intestinal ischaemia was subsequently confirmed at laparotomy when an internal hernia with a distal small bowel volvulus and necrosis was found. Intestinal ischaemia presenting with a life‐threatening cardiac dysrhythmia in a child appears not to have been reported previously.
Review article: Coronary artery stenoses: Detection and revascularization in renal disease
Authors: PILMORE HELEN L 
Published: June 2009

SUMMARYCardiovascular events are markedly elevated in those with all degrees of renal impairment compared to the general population. There are well established guidelines in the general population for the management of coronary artery disease, however, similar guidelines have not been established in the renal population. This review examines the current published work on the detection of coronary artery stenoses in addition to summarizing the outcomes of revascularization in patients with kidney disease. Testing for coronary artery disease in the renal population most commonly occurs in dialysis patients as part of their assessment for renal transplantation. While a positive myocardial stress test for the detection of significant coronary artery stenoses is associated with an increased risk of cardiac events, there is no clear information currently showing that cardiovascular testing itself reduces the rate of adverse cardiac events after transplantation. Revascularization of coronary artery stenoses is associated with higher morbidity and mortality in all groups with kidney disease than in the general population, with the exception of renal transplant recipients where the mortality is likely to be similar to that of the general population. There appears to be a benefit in coronary artery bypass surgery compared to percutaneous intervention in those on dialysis and after renal transplant. Currently, there is little data to support coronary artery intervention prior to transplantation in those with asymptomatic coronary artery disease.
Experimental warming causes rapid loss of plant diversity in New England salt marshes
Authors: Gedan Keryn B. , Bertness Mark D. 
Published: June 2009

AbstractAnthropogenic climate change is predicted to cause widespread biodiversity loss due to shifts in species’ distributions, but these predictions rarely incorporate ecological associations such as zonation. Here, we predict the decline of a diverse assemblage of mid‐latitude salt marsh plants, based on an ecosystem warming experiment. In New England salt marshes, a guild of halophytic forbs occupies stressful, waterlogged pannes. At three sites, experimental warming of < 4 °C led to diversity declines in pannes and rapid takeover by a competitive dominant, Spartina patens. In Rhode Island, near their southern range limit, pannes were more sensitive to warming than farther north, and panne area also declined in control plots over the three‐season experiment. These results suggest that warming will rapidly reduce plant diversity in New England salt marshes by eliminating a high diversity zone. Biodiversity in zoned ecosystems may be more affected by climate‐driven shifts in zonation than by individual species’ distribution shifts.
When can we distinguish between neutral and non‐neutral processes in community dynamics under ecological drift?
Authors: Ruokolainen Lasse , Ranta Esa , Kaitala Veijo , Fowler Mike S. 
Published: June 2009

AbstractDetermining whether the composition of ecological communities (species presence and abundance), can be predicted from species demographic traits, rather than being a result of neutral drift, is a key ecological question. Here we compare the similarity of community composition, from different community assembly models run under identical environmental conditions, where interspecific competition is assumed to be either neutral or niche‐based. In both cases, species colonize a focal patch from a network of neighbouring patches in a metacommunity. We highlight the circumstances (rate and spatial scale of dispersal, and the relative importance of ecological drift) where commonly used community similarity metrics or species rank–abundance relationships are likely to give similar results, regardless of the underlying processes (neutral or non‐neural) driving species’ dynamics. As drift becomes more important in driving species abundances, deterministic niche structure has a smaller influence. Our ability to discriminate between different underlying processes driving community organization depends on the relative importance of different drift processes that operate on different spatial scales.
The ‘Draw‐the‐Family Test’ in the preoperative assessment of patients with anorectal diseases and psychological distress: a prospective controlled study
Authors: Miliacca C. , Gagliardi G. , Pescatori M. 
Published: June 2009

AbstractAim  Some benign anorectal diseases may have psychosomatic aetiology, but patients often refuse direct psychological counselling. The Draw‐the‐Family Test (DFT) is a simple indirect investigation. The aim of this study was to evaluate the DFT in patients with psychological problems undergoing surgery for benign anorectal disease and to correlate the results with surgical outcome.Method  DFT was administered prior to surgery to 62 patients with benign anorectal disease who admitted psychological problems at the time of the outpatient visit. Of these 18 (29%) had functional disease, mainly obstructed defecation (OD) while 44 (71%) had organic disease (haemorrhoids, fissures, pilonidal sinus or fistula). DFT was also administered to 40 healthy control subjects. Each DFT was judged as normal or pathological according to 10 parameters. Patients were followed up for a median of 12 months (range 3–64) and divided into two outcome groups, success (n = 58) and failure (n = 12) according to the results of a questionnaire. The DFT of all patients was then correlated with the outcome.Results  None of the patients refused DFT. All DFT parameters but one (animal/things instead of human beings) were more frequent in patients compared with controls (P < 0.05). When comparing separately organic or functional disease patients with controls, one parameter (absence of patient in the drawing) was only pathological in the organic disease group (P < 0.05). Another parameter (schematic figures) was more frequently altered in the organic disease group compared with the functional disease group (P = 0.01). Eight out of 10 parameters were more frequently pathological in patients who failed after treatment, but none reached statistical significance.Conclusion  Results of DFT in patients with anorectal disease admitting to psychological problems are markedly different from healthy controls. Patients with organic disease and those with functional bowel disease have different DFT profiles. In our study group, DFT had an excellent compliance but could not predict the outcome of surgery.