bluuebunny/crossref_metadata_2025_split huggingface dataset:
Postoperative emesis after laparoscopic pyloromyotomy in infantile hypertrophic pyloric stenosis
Authors: Castellani C , Peschaut T , Schippinger M , Saxena AK 
Published: October 2013

AbstractAimThis study aimed to determine the causes of postoperative emesis (PE) in neonates with infantile hypertrophic pyloric stenosis (IHPS) after laparoscopic pyloromyotomy (LP).MethodsRetrospective review of the hospital database for infants with IHPS managed between 2000 and 2010 was performed. Relevant data were collected from the clinical records in the Medocs® system and used for statistical analysis.ResultsDuring the 10‐year period, 95 patients with IHPS were identified and 43 (36 boys and seven girls) fulfilled the inclusion criteria. PE occurred in 21 infants (48.8%), of which nine presented with manifestations of enteric infections, with confirmed diagnosis in four. PE was significantly higher in the fast track feeding protocol (FTFP) group 12/15 compared with the conventional slow feeding protocol (CSFP) group 8/21 (p = 0.019). Gastro‐oesophageal reflux (GER) confirmed by 24‐h impedance monitoring was responsible for PE in three. Operative revision for suspected incomplete pyloromyotomy was performed in five infants. However, incomplete myotomy could only be confirmed in two infants during surgery.ConclusionPostoperative emesis in IHPS after LP requires careful evaluation as it can be a result of enteric viral infections, aggressive feeding protocols or GER. Decisions to perform reoperations for incomplete myotomy after LP due to PE are challenging.
The relationship between body growth and pulmonary function in children with cystic fibrosis
Authors: Woestenenk Janna W , Stellato Rebecca K , Terheggen−Lagro Suzanne W , van der Ent Cornelis K , Houwen Roderick HJ 
Published: October 2013

AbstractAimTo measure the weight and height of children with cystic fibrosis (CF) from 2 to 10 years of age and to investigate the relationship between these parameters and forced expiratory volume in 1 sec (FEV1) beginning at 6 years of age.MethodsWeight and height were expressed as z‐scores for weight‐for‐age (WFA), height‐for‐age (HFA), height‐adjusted‐for‐target‐height (HFA/TH) and weight‐for‐height (WFH). The children were categorised as having a z−score ≥0, between 0 and −1, or <−1 based on z‐scores at 2 years of age. The cross‐sectional and longitudinal relationships between FEV1 and WFA, HFA, HFA/TH and WFH were determined and the predictive value of these parameters for FEV1.ResultsWe enrolled 156 CF children. Their mean weight and height were below the average for the healthy population. Both WFA and WFH increased with age (primarily before the age of 6), while the reduction in HFA and HFA/TH persisted. Importantly, the yearly decline in FEV1 was significantly slowed [by 1.8 and 1.9% for each unit increase in WFA and WFH (p < 0.015)] in children who gained weight.ConclusionCF patients aged 2 to 10 years have long‐term impaired growth. Nevertheless, weight gain slowed the decline in FEV1 in these patients.
Lipotoxicity and the role of maternal nutrition
Authors: Pruis M. G. M. , van Ewijk P. A. , Schrauwen‐Hinderling V. B. , Plösch T. 
Published: October 2013

AbstractIntrauterine malnutrition predisposes the offspring towards the development of type 2 diabetes and cardiovascular disease. To explain this association, the Developmental Origins of Health and Disease hypothesis was introduced, meaning that subtle environmental changes during embryonic and foetal development can influence post‐natal physiological functions. Different mechanisms, including epigenetics, are thought to be involved in this foetal programming, but the link between epigenetics and disease is missing. There is increasing evidence that ectopic lipid accumulation and/or lipotoxicity is induced by foetal programming. The aim of this review is to provide insights into the mechanisms underlying lipotoxicity through programming, which contributes to the increase in hepatic and cardiac metabolic risk.
Adenosine increases LPS‐induced nuclear factor kappa B activation in smooth muscle cells via an intracellular mechanism and modulates it via actions on adenosine receptors
Authors: Yang J. , Zheng X. , Haugen F. , Darè E. , Lövdahl C. , Schulte G. , Fredholm B. B. , Valen G. 
Published: October 2013

AbstractAimIn inflamed and damaged cardiovascular tissues, local extracellular adenosine concentrations increase coincidentally with activation of the transcription factor nuclear factor kappa B (NFκB). To investigate whether adenosine influences NFκB activation in vascular smooth muscle cells (VSMCs) and, if so, to examine the role of its receptors.MethodsVSMCs were isolated from NFκB–luciferase reporter mice, cultured and then treated by lipopolysaccharide (LPS) to activate NFκB signalling. Adenosine, adenosine receptor agonists and antagonists, adenosine deaminase and uptake inhibitors were used together with LPS to evaluate the role of adenosine and its receptors on NFκB activation, which was assessed by luciferase activity and NFκB target gene expression.ResultsAdenosine potentiated LPS‐induced NFκB activation. This was dependent on adenosine uptake and enhanced by an adenosine deaminase inhibitor, suggesting that intracellular adenosine plays an important role. Non‐selective adenosine receptor agonists (2Cl‐Ado and NECA) inhibited NFκB activation induced by LPS. Selective A1 or A2A antagonist given alone could not completely antagonize the NECA effect, indicating that the inhibitory effect was due to multiple adenosine receptors. The activation of the A3 receptor further increased LPS‐induced NFκB activation.ConclusionsAdenosine increases LPS‐induced nuclear factor kappa B activation in smooth muscle cells via an intracellular mechanism and decreases it via actions on A1 and A2A receptors. These results provide novel insights into the role of adenosine as a regulator of inflammation‐induced NFκB activation.
Autophagy is altered in skeletal and cardiac muscle of spontaneously hypertensive rats
Authors: Bloemberg D. , McDonald E. , Dulay D. , Quadrilatero J. 
Published: October 2013

AbstractAimAutophagy is a subcellular degradation mechanism important for muscle maintenance. Hypertension induces well‐characterized pathological changes to the heart and is associated with impaired function and increased apoptotic signalling in skeletal muscle. We examined whether essential hypertension affects several autophagy markers in skeletal and cardiac muscle.MethodsImmunoblotting and qRT‐PCR were used to measure autophagy‐related proteins/mRNA in multiple skeletal muscles as well as left ventricle (LV) of spontaneously hypertensive rats (SHR) and normotensive Wistar–Kyoto rats (WKY).ResultsSkeletal muscles of hypertensive rats had decreased (P < 0.01) cross‐sectional area of type I fibres (e.g. soleus WKY: 2952.9 ± 64.4 μm2 vs. SHR: 2579.9 ± 85.8 μm2) and a fibre redistribution towards a ‘fast’ phenotype. Immunoblot analysis revealed that some SHR skeletal muscles displayed a decreased LC3II/I ratio (P < 0.05), but none showed differences in p62 protein. LC3 and LAMP2 mRNA levels were increased approx. 2–3‐fold in all skeletal muscles (P < 0.05), while cathepsin activity, cathepsin L mRNA and Atg7 protein were increased 16–17% (P < 0.01), 2–3‐fold (P < 0.05) and 29–49% (P < 0.01), respectively, in fast muscles of hypertensive animals. Finally, protein levels of BAG3, a marker of chaperone‐assisted selective autophagy, were 18–25% lower (P < 0.05) in SHR skeletal muscles. In the LV of SHR, LC3I and p62 protein were elevated 34% (P < 0.05) and 47% (P < 0.01), respectively. Furthermore, p62 mRNA was 68% higher (P < 0.05), while LAMP2 mRNA was 45% lower (P < 0.05), in SHR cardiac muscle. There was no difference in Beclin1, Atg7, Bnip3 or BAG3 protein in the LV between strains.ConclusionThese results suggest that autophagy is altered in skeletal and cardiac muscle during hypertension.
PPARγ activation inhibits cerebral arteriogenesis in the hypoperfused rat brain
Authors: Duelsner A. , Gatzke N. , Hillmeister P. , Glaser J. , Zietzer A. , Nagorka S. , Janke D. , Pfitzner J. , Stawowy P. , Meyborg H. , Urban D. , Bondke Persson A. , Buschmann I. R. 
Published: October 2013

AbstractAimsPPARγ stimulation improves cardiovascular (CV) risk factors, but without improving overall clinical outcomes. PPARγ agonists interfere with endothelial cell (EC), monocyte and smooth muscle cell (SMC) activation, function and proliferation, physiological processes critical for arterial collateral growth (arteriogenesis). We therefore assessed the effect of PPARγ stimulation on cerebral adaptive and therapeutic collateral growth.MethodsIn a rat model of adaptive cerebral arteriogenesis (3‐VO), collateral growth and function were assessed (i) in controls, (ii) after PPARγ stimulation (pioglitazone 2.8 mg kg−1; 10 mg kg−1 compared with metformin 62.2 mg kg−1 or sitagliptin 6.34 mg kg−1) for 21 days or (iii) after adding pioglitazone to G‐CSF (40 μg kg−1 every other day) to induce therapeutic arteriogenesis for 1 week. Pioglitazone effects on endothelial and SMC morphology and proliferation, monocyte activation and migration were studied.ResultsPPARγ stimulation decreased cerebrovascular collateral growth and recovery of hemodynamic reserve capacity (CVRC controls: 12 ± 7%; pio low: −2 ± 9%; pio high: 1 ± 7%; metformin: 9 ± 13%; sitagliptin: 11 ± 12%), counteracted G‐CSF‐induced therapeutic arteriogenesis and interfered with EC activation, SMC proliferation, monocyte activation and migration.ConclusionPharmacologic PPARγ stimulation inhibits pro‐arteriogenic EC activation, monocyte function, SMC proliferation and thus adaptive as well as G‐CSF‐induced cerebral arteriogenesis. Further studies should evaluate whether this effect may underlie the CV risk associated with thiazolidinedione use in patients.
The adrenergic regulation of proximal tubular Na+/H+ exchanger 3 in the rat
Authors: Healy V. , Thompson C. , Johns E. J. 
Published: October 2013

AbstractAimThis study in the anaesthetized rat investigated how renal sympathetic nerve activity and catecholamine release influenced NHE3 abundance and activity in proximal tubular brush border membranes using both in vivo and in vitro approaches.MethodsRenal excretory function and brush border NHE3 abundance and activity were measured in rat kidneys which underwent renal denervation, renal nerve electrical stimulation and renal infusion of phenylephrine and the NHE3 inhibitor S1661. NHE3 activity and cell surface abundance were also measured in primary cultures of proximal tubular cells treated with noradrenaline and prazosin.ResultsAcute renal denervation caused a natriuresis and diuresis, which occurred with a reduction in NHE3 abundance and activity in the brush border membranes. By contrast, low‐level electrical stimulation of the renal innervation causing an antinatriuresis and antidiuresis increased NHE3 activity in the brush border membranes. Intrarenal infusion of phenylephrine caused an antinatriuresis and antidiuresis, while blockade of NHE3 activity, using local infusion of the blocker S1661, caused a natriuresis and diuresis. Exposure of primary cultures of proximal tubular cells to noradrenaline increased brush border NHE3 abundance and activity which was blocked by prior exposure to prazosin, indicating it as an α1‐adrenoceptor‐mediated mechanism.ConclusionTogether, these findings demonstrate that the renal sympathetic nerves not only have a direct action to modulate tubular sodium reabsorption via stimulation of the NHE transporter, but also have an indirect effect, whereby NHE3 abundance is increased within the brush border membrane, thereby increasing the capacity for fluid reabsorption.
Investigation of child maltreatment: Survey among junior school pupils in Henan province of China
Authors: Shen Lijuan , Zhang Yingli , Liang Wei , Zhang Yalin 
Published: October 2013

AbstractIntroductionThis study is to examine the prevalence of child maltreatment and its association with attachment and self‐esteem among junior schools students in Henan province of China.MethodsSeven hundred thirty‐six pupils were selected from two public schools. Data were collected with the self‐reported questionnaires of the basic demographic information, the Revised Inventory of Parent and Peer Attachment, the Rosenberg Self‐Esteem Scale, and the Childhood Trauma Questionnaire. Data were analyzed using SPSS 17.0.ResultIn this study, the prevalence of emotional neglect, physical neglect, sexual abuse, emotional abuse, and physical abuse were 22.8%, 38.0%, 11.0%, 10.6%, and 7.1%, respectively. There was a significant difference between male and female pupils in the prevalence of the physical neglect (Pearson χ2 = 16.27, P < 0.01), sexual abuse (χ2 = 15.38, P < 0.01), and physical abuse (χ2 = 11.55, P < 0.01). In addition, physical neglect was the most common reported by pupils in the child maltreatment. Drinking habit of the mother was a significantly risk factor for emotional abuse, emotional neglect, and physical neglect.ConclusionChild abuse is still a severe social and psychological problem, and child neglect is more common than child abuse. It is noteworthy that mothers with drinking habit were more likely to abuse their own children than fathers with drinking habit.
Review article: the association of diet with onset and relapse in patients with inflammatory bowel disease
Authors: Spooren C. E. G. M. , Pierik M. J. , Zeegers M. P. , Feskens E. J. M. , Masclee A. A. M. , Jonkers D. M. A. E. 
Published: October 2013

SummaryBackgroundThe role of diet in inflammatory bowel disease (IBD) is supported by migration studies and increasing incidences in line with Westernisation.AimTo give a complete overview of studies associating habitual diet with the onset or relapses in ulcerative colitis (UC) or Crohn's disease (CD).MethodsA structured search in Pubmed, the Cochrane Library and EMBASE was performed using defined key words, including only full text papers in English language.ResultsForty‐one studies were identified, investigating onset (n = 35), relapses (n = 5) or both (n = 1). Several studies reported high intake of sugar or sugar‐containing foods (n = 7 UC, n = 12 CD), and low intake of fruits and/or vegetables (n = 5 UC, n = 10 CD) to be associated with an increased onset risk. However, these findings could not be confirmed by similar or higher numbers of other studies. A possible protective role was found for grain‐derived products in CD onset, but results were inconsistent for dietary fibre in UC and CD and grain‐derived products in UC. No definite conclusions could be drawn for unsaturated fatty acids (UFA), protein and energy intake due to limited and/or inconsistent results. Six studies reported on diet and relapse risk, of which only two (n = 1 UC, n = 1 CD) had a prospective follow‐up.ConclusionsThe current evidence is not sufficient to draw firm conclusions on the role of specific food components or nutrients in the aetiology of IBD. Furthermore, large prospective studies into the role of habitual diet as a trigger of relapses are needed, to identify new therapeutic or preventive targets.
A trial of mercaptopurine is a safe strategy in patients with inflammatory bowel disease intolerant to azathioprine: an observational study, systematic review and meta‐analysis
Authors: Kennedy N. A. , Rhatigan E. , Arnott I. D. R. , Noble C. L. , Shand A. G. , Satsangi J. , Lees C. W. 
Published: October 2013

SummaryBackgroundThiopurines maintain remission and modify disease course in inflammatory bowel disease. Use is limited by intolerance and subsequent drug withdrawal in approximately 17% of patients treated with azathioprine. Previous case series have addressed the success rates of re‐treatment with mercaptopurine in these individuals.AimsTo determine the rate of tolerance when trialling mercaptopurine in azathioprine‐intolerant patients and the factors predictive of success, and to perform a systematic review and meta‐analysis of these data with other published data sets.MethodsA retrospective observational study of 149 patients with IBD (82 with Crohn's disease and 67 with ulcerative colitis) previously intolerant of azathioprine subsequently treated with mercaptopurine was performed. A meta‐analysis was undertaken of all published studies of mercaptopurine use in azathioprine‐intolerant patients (455 patients in 11 included studies).ResultsMercaptopurine was tolerated by 58% of azathioprine‐intolerant patients in the Edinburgh cohort. In the meta‐analysis, 68% tolerated mercaptopurine. A higher proportion of those in the meta‐analysis with GI toxicity (62%) or hepatotoxicity (81%) were able to tolerate mercaptopurine than those with flu‐like illness (36%). Among those patients who ceased mercaptopurine for further adverse effects, 59% experienced the same adverse effect as they had with azathioprine.ConclusionsThis meta‐analysis shows that switching to mercaptopurine is a safe therapeutic strategy for over two‐thirds of azathioprine‐intolerant patients and may help optimise immunomodulatory therapy in inflammatory bowel disease. A trial of mercaptopurine should be attempted in IBD patients (except those with acute pancreatitis or bone marrow aplasia) before considering thiopurine intolerance.
The outcome of patients with oesophageal eosinophilic infiltration after an eight‐week trial of a proton pump inhibitor
Authors: Vazquez‐Elizondo G. , Ngamruengphong S. , Khrisna M. , DeVault K. R. , Talley N. J. , Achem S. R. 
Published: October 2013

SummaryBackgroundCurrent diagnostic guidelines recommend that eosinophilic oesophagitis (EoE) should be diagnosed only after GERD is excluded by a lack of response to a trial of acid suppression. There is limited information available providing outcome data about the effectiveness of this approach.AimTo examine the impact of double‐dose proton pump inhibitor (PPI) therapy on symptoms, endoscopic and histological features in patients with documented oesophageal eosinophilia consistent with EoE (≥15 eosinophils/high‐power field).MethodsSixty consecutive symptomatic patients with documented oesophageal eosinophilia received open‐label omeprazole 20 mg orally twice daily before meals for 8 weeks. Clinical, endoscopic and histological (resolution: 0–5 eosinophils/HPF, partial improvement: 5–14 eosinophils/HPF), or no improvement: (≥15 eosinophils/HPF) evaluation was repeated at the end of this period. An expert GI pathologist, unaware of the study aims, reviewed all slides.ResultsClinical improvement occurred in 43 (71.6%), endoscopic signs were reduced in 34 (61.8%) and normalised in 12 (21.8%), and histologically, 34 (56.6%) improved, while 15 (25%) obtained complete resolution. Overall, 22 patients (36.7%) obtained both complete clinical and histological remission.ConclusionsMore than 50% of patients with documented oesophageal eosinophilic infiltration in the EoE range improved when treated with a double‐dose PPI trial for 8 weeks. These findings support the published guidelines recommending a PPI trial prior to diagnosing EoE, and confirm the existence of an eosinophilic oesophageal infiltrationPPI‐responsive population.
Impact of mid‐successional dominant species on the diversity and progress of succession in regenerating temperate grasslands
Authors: Bartha Sándor , Szentes Szilárd , Horváth András , Házi Judit , Zimmermann Zita , Molnár Csaba , Dancza István , Margóczi Katalin , Pál Róbert W. , Purger Dragica , Schmidt Dávid , Óvári Miklós , Komoly Cecília , Sutyinszki Zsuzsanna , Szabó Gábor , Csathó András István , Juhász Melinda , Penksza Károly , Molnár Zsolt 
Published: October 2013

AbstractQuestions(i) Which species dominate mid‐successional old‐fields in Hungary? How does the identity of these species relate to local (patch‐scale) diversity and to the progress of succession? (ii) Which species have the strongest negative impact on diversity in spontaneous old‐field succession and what generalizations are possible about traits of these species? (iii) Are these species dominant or subordinate components in mature target communities? (iv) Do native or alien species have stronger effects on the diversity and progress of succession?LocationAbandoned agricultural fields (abandoned croplands, orchards and vineyards) at various locations throughout Hungary.MethodsVegetation patterns on 112 old‐fields, in 25 sites varying in soil and climatic conditions, topography, landscape contexts and land‐use histories were sampled. Most old‐fields had appropriate seed sources in the immediate vicinity, i.e. natural or semi‐natural grasslands (meadows steppes, closed and open sand steppes) as source and target habitats. Age of abandoned fields ranged from 1 to 69 yr, but most sites were between 15 and 60 yr. The cover of vascular plant species (%) was estimated in 2 × 2‐m plots. Relationships between diversity, progress of succession (similarity to target communities) and identity of dominants were tested.ResultsA small portion of successional dominants (eight species) had strong negative impacts on diversity. These species belonged to Poaceae, Asteraceae and Fabaceae. Most of these species were wind‐pollinated, and capable of lateral vegetative spread. Dominant species varied in size and had, on average, a low requirement for N but a high requirement for light. With one exception, Solidago gigantea, they were native to the Hungarian flora. Significant differences were found among the impact of successional dominants when dominant species were grouped according to their original role (dominants or subordinates) in natural communities. The overall effect of species identity was also significant. Bothriochloa ischaemum was identified as the species with the strongest negative effect on species diversity.ConclusionsOur results suggest that mid‐successional dominant species differ in their impact on diversity and progress of succession. Mid‐successional plots dominated by alien species, or by native species that were originally subordinate in natural communities, regenerate less successfully and may temporarily arrest succession. Therefore, early colonization of native dominants should be enhanced with restoration measures.
Role of Platelets in Inflammation and Cancer: Novel Therapeutic Strategies
Authors: Dovizio Melania , Alberti Sara , Guillem‐Llobat Paloma , Patrignani Paola 
Published: October 2013

AbstractPlatelets play a central role in inflammation through their direct interaction with other cell types, such as leucocytes and endothelial cells, and by the release of many factors, that is, lipids [such as thromboxane (TX)A2] and proteins (a wide number of angiogenic and growth factors) stored in α‐granules, and adenosine diphosphate (ADP), stored in dense granules. These platelet actions trigger autocrine and paracrine activation processes that lead to leucocyte recruitment into different tissues and phenotypic changes in stromal cells which contribute to the development of different disease states, such as atherosclerosis and atherothrombosis, intestinal inflammation and cancer. The signals induced by platelets may cause pro‐inflammatory and malignant phenotypes in other cells through the persistent induction of aberrant expression of cyclooxygenase (COX)‐2 and increased generation of prostanoids, mainly prostaglandin (PG)E2. In addition to cardiovascular disease, enhanced platelet activation has been detected in inflammatory disease and intestinal tumourigenesis. Moreover, the results of clinical studies have shown that the antiplatelet drug aspirin reduces the incidence of vascular events and colorectal cancer. All these pieces of evidence support the notion that colorectal cancer and atherothrombosis may share a common mechanism of disease, that is, platelet activation in response to epithelial (in tumourigenesis) and endothelial (in tumourigenesis and atherothrombosis) injury. Extensive translational medicine research is necessary to obtain a definitive mechanistic demonstration of the platelet‐mediated hypothesis of colon tumourigenesis. The results of these studies will be fundamental to support the clinical decision to recommend the use of low‐dose aspirin, and possibly other antiplatelet agents, in primary prevention, that is, even for individuals at low cardiovascular risk.