bluuebunny/crossref_metadata_2025_split huggingface dataset:
Indirect Ion Selective Electrode Methods Potentially Overestimate Peritoneal Dialysate Sodium Losses
Authors: Persaud Jahm , Thomas Michael , Davenport Andrew 
Published: November 2013

AbstractMeasurements of dialysate sodium are used to estimate peritoneal dialysis sodium losses and sodium sieving, a measure of hydraulic permeability of the peritoneum. Peritoneal dialysates differ from serum samples in terms of pH, osmolality, protein and glucose concentration. We wished to determine whether these factors affected sodium measurement. Dialysate samples were taken from 52 consecutive peritoneal dialysis patients attending for a standard peritoneal dialysis equilibrium test (PET), 20 with standard lactate dialysate and 32 with neutral pH dialysate and sodium was measured by both flame photometry and indirect ion selective electrode (ISE). Sodium measured by ISE consistently overestimated that measured by flame photometer, mean bias 1.5 mmol/L (95% confidence limits 1.2 to 1.8), P < 0.001. Sodium was lower in fresh neutral pH dialysates by both methods – flame 125.3 ± 1.17 vs. 131.6 ± 0.39 mmol/L, than standard lactate dialysates ISE 127.4 ± 1.05 vs 132.7 ± 0.27 mmol/L, P < 0.001. Glucose was higher in fresh neutral pH dialysates 122.7 ± 1.1 vs. standard lactate dialysates 116.7 ± 0.4 mmol/L, P < 0.001. On multiple regression analysis, only glucose was found to be an independent factor for sodium measurement, F = 14.78, β = −0.0851, SEM 0.022, 95% confidence limits −1.28 to −0.042. In this study there was a small but consistent difference between sodium measurements by ISE and flame photometry during the PET. Sodium measurements by either method appeared to be affected by hypertonic dialysates, but there were differences with pH. This may potentially lead to errors in both overestimating peritoneal sodium losses and the proportion of patients with ultrafiltration failure due to loss of sodium sieving.
Parachute Implant: CT Morphological Criteria of our Center to Identify the Suitable Patient
Authors: Bozdag‐Turan Ilkay , Bermaoui Benjamin , Turan R. Goekmen , Kische Stephan , Paranskaya Liliya , Kloker Katja , Ortak Jasmin , Akin Ibrahim , Hauenstein Karlheinz , Nienaber Christoph A. , Ince Hueseyin 
Published: November 2013

SummaryAimsIn this study, we present and discuss our institutionalized and standardized computed tomography (CT) morphological criteria for the treatment of patients with a parachute device.Methods and ResultsAfter clinical and echocardiographic screening of 79 patients with ischemic heart failure, 28 were examined using multidetector computed tomography (MDCT) to assess their suitability for treatment with a parachute implant. From the 28 examined patients, nine were suitable for parachute implantation. Within the group of excluded patients, the cardiac diameters of one‐third of the patients were too large, whereas for another third they were too small. Approximately 20% of the patients were rejected because of a deep insertion of the papillary muscles. Further reasons included left ventricular bands as well as mismatches between CT and echocardiographic measurements of left ventricular ejection fraction (LVEF).ConclusionsTo ensure a safe parachute device implantation in patients with ischemic heart failure, only the CT at present offers the capability to obtain complete and dynamic three‐dimensional (3D) measurements of the cardiac dimensions.
Childhood maltreatment and inflammatory markers: a systematic review
Authors: Coelho R. , Viola T. W. , Walss‐Bass C. , Brietzke E. , Grassi‐Oliveira R. 
Published: November 2013

ObjectiveChildhood maltreatment (CM) has been associated with several diseases in adult life, including diabetes, obesity and mental disorders. Inflammatory conditions have been postulated as possible mediators of this relationship. The aim was to conduct a systematic review regarding the association between CM and inflammatory markers in adulthood.MethodA literature search of the PubMed, ISI, EMBASE and PsychINFO databases was conducted. The key terms used were as follows: ‘Child Maltreatment’, ‘Childhood Trauma’, ‘Early Life Stress’, ‘Psychological Stress’, ‘Emotional Stress’, ‘Child Abuse’ and ‘Child Neglect’. They were cross‐referenced separately with the terms: ‘C‐reactive Protein (CRP)’, ‘Tumor Necrosis Factor’, ‘Cytokine’, ‘Interleukin’, ‘Inflammatory’ and ‘Inflammation’.ResultsTwenty articles remained in the review after exclusion criteria were applied. Studies showed that a history of CM was associated with increased levels of CRP, fibrinogen and proinflammatory cytokines. Increased levels of circulating CRP in individuals with a history of CM were the most robust finding among the studies. Data about anti‐inflammatory mediators are still few and inconsistent.ConclusionChildhood maltreatment is associated with a chronic inflammatory state independent of clinical comorbidities. However, studies are heterogeneous regarding CM assessment and definition. Important methodological improvements are needed to better understand the potential impact of CM on inflammatory response.
Progesterone Activates Multiple Innate Immune Pathways in Chlamydia trachomatis‐Infected Endocervical Cells
Authors: Wan Charles , Latter Joanna L. , Amirshahi Ashkan , Symonds Ian , Finnie Jane , Bowden Nikola , Scott Rodney J. , Cunningham Kelly A. , Timms Peter , Beagley Kenneth W. 
Published: November 2013

ProblemSusceptibility to Chlamydia trachomatis infection is increased by oral contraceptives and modulated by sex hormones. We therefore sought to determine the effects of female sex hormones on the innate immune response to C. trachomatis infection.Method of studyECC‐1 endometrial cells, pre‐treated with oestradiol or progesterone, were infected with C. trachomatis and the host transcriptome analysed by Illumina Sentrix HumanRef‐8 microarray. Primary endocervical epithelial cells, prepared at either the proliferative or secretory phase of the menstrual cycle, were infected with C. trachomatis and cytokine gene expression determined by quantitative RT‐PCR analysis.ResultsChlamydia trachomatis yield from progesterone‐primed ECC‐1 cells was significantly reduced compared with oestradiol‐treated cells. Genes upregulated in progesterone‐treated and Chlamydia‐infected cells only included multiple CC and CXC chemokines, IL‐17C, IL‐29, IL‐32, TNF‐α, DEFB4B, LCN2, S100A7‐9, ITGAM, NOD2, JAK1, IL‐6ST, type I and II interferon receptors, numerous interferon‐stimulated genes and STAT6. CXCL10, CXCL11, CX3CL1 and IL‐17C, which were also upregulated in infected secretory‐stage primary cells, and there was a trend towards higher levels of immune mediators in infected secretory‐phase compared with proliferative‐phase cells.ConclusionProgesterone treatment primes multiple innate immune pathways in hormone‐responsive epithelial cells that could potentially increase resistance to chlamydial infection.
Carotid Artery Doppler Flow Pattern After Deep Hypothermic Circulatory Arrest in Neonatal Piglets
Authors: Tirilomis Theodor , Malliarou Stella , Coskun K. Oguz , Schoendube Friedrich A. 
Published: November 2013

AbstractThe mechanisms of cerebral injury after cardiac surgery in neonates are not clear. The aim of the study was the analysis of flow changes in the carotid artery of neonatal piglets after deep hypothermic circulatory arrest (DHCA). Eight neonatal piglets were connected to cardiopulmonary bypass (CPB) and underwent (i) cooling to 18°C core temperature within 30 min, (ii) DHCA for 90 min, and finally (iii) rewarming to 37°C after cross‐clamp release (60 min of reperfusion). The blood flow was measured in the left carotid artery by an ultrasonic flow probe before CPB (baseline; T0), immediately after termination of reperfusion on CPB (T1), 30 min later (T2), and 60 min later (T3). Additionally, the pulsatility index and the resistance index were calculated and compared. Finally, the relationship between the carotid artery flow and the corresponding pressure at each time‐point was compared. After termination of CPB (T1), the mean carotid artery flow was reduced from 45.26 ± 2.58 mL/min at baseline to 23.29 ± 2.58 mL/min (P < 0.001) and remained reduced 30 and 60 min later (P < 0.001 vs. baseline). Both the pulsatility index and the resistance index were increased after termination of reperfusion, with the maximum occurring 30 min after CPB end. In conclusion, the carotid artery Doppler flow in neonatal piglets was reduced after DHCA, while the indices of pulsatility and resistance increased.
Bone mineral density in Turner's syndrome and the influence of pubertal development
Authors: Nadeem Montasser , Roche Edna F 
Published: November 2013

AbstractAimTo describe bone mineral density at the lumbar spine in a group of girls with Turner's syndrome and determine its relation to pubertal development.MethodsGirls with Turner's syndrome aged over 12 years were invited to participate in the study. All participants underwent auxology, pubertal assessment and laboratory evaluation. Bone mineral density was estimated by dual‐energy X‐ray absorptiometry. Bone mineral apparent density was then calculated, and the results were compared with age‐matched Dutch reference data.ResultsWe studied 32 girls with Turner's syndrome, mean (SD) [range] age 16.7 (2.6) [12.4–20.2] years and height 148.3 (9.0) [126–159.2] cm. Bone mineral apparent density lumbar spine values were −0.87 SD, significantly lower than in the reference population (p <0.001). Bone mineral apparent density values were positively and significantly associated with breast Tanner stages and postmenarcheal status, but not spontaneous puberty. However, no significant association was found between bone mineral apparent density and karyotype, growth hormone or timing of oestrogen therapy.ConclusionGirls with Turner's syndrome have lower bone mineral apparent density values at the lumbar spine, even after correcting for size, compared with an age‐ and sex‐matched general population. Pubertal development has significant impact on bone mineral apparent density in girls with Turner's syndrome.
Actions of intravenous injections of AVP and oxytocin on plasma ACTH, GH, insulin and glucagon concentrations in goats
Authors: Roh Sang‐gun , Koiwa Kohta , Sato Katsuyoshi , Ohtani Yoshihisa , Takahashi Tatsuyuki , Katoh Kazuo 
Published: November 2013

AbstractThis study was conducted to investigate the arginine‐vasopressin (AVP)‐ and oxytocin‐induced changes in plasma adrenocorticotropic hormone (ACTH), growth hormone (GH), insulin and glucagon levels and their metabolite concentrations in goats. In this study, five goats were intravenously injected with either AVP (0.3 nmol/kg body weight (BW)) or oxytocin (0.7 IU/kg BW). AVP injection significantly increased ACTH and GH secretions compared to controls, although insulin and glucagon concentrations were not altered. The incremental areas (ICAs) of the ACTH and GH concentrations were higher in the AVP group than in the saline group. Oxytocin injections increased insulin and glucagon secretions, while ACTH level was not altered. GH levels became elevated 30 min after the oxytocin injection. The ICAs of insulin and glucagon after oxytocin was injected were higher than those of the control. Results indicate that AVP is a potent stimulant of ACTH and GH secretions, while oxytocin uses different pathways to regulate insulin and glucagon secretions in goats.
Sex hormones and biomarkers of neuroprotection and neurodegeneration: implications for female reproductive events in bipolar disorder
Authors: Frey Benicio N , Dias Rodrigo S 
Published: November 2013

ObjectivesPrevious studies have suggested that women with bipolar disorder are at higher risk for mood episodes during periods of intense hormonal fluctuation (e.g., premenstrual, postpartum, perimenopause). There is converging literature showing that estrogen and progesterone can modulate neurotransmitter systems and intracellular signaling pathways known to be affected by mood stabilizing agents. Here, we critically review clinical aspects of reproductive cycle events in women with bipolar disorder and preclinical studies, with a focus on the functional interactions between sex hormones and biomarkers of neuroprotection and neurodegeneration that are thought to be involved in the neurobiology of bipolar disorder: brain‐derived neurotrophic factor, oxidative stress, and inflammation.MethodsA MedLine search usingestrogen,progesterone,brain‐derived neurotrophic factor,oxidative stress, andinflammationas key words was conducted.ResultsData showed that estrogen and progesterone closely interact with brain‐derived neurotrophic factor, oxidative stress, and inflammation pathways.ConclusionsThis relationship between sex hormones and the pathways of neuroprotection/neurodegeneration may be relevant to the psychopathological aspects of bipolar disorder in women.
Prognostic and diagnostic implications of epithelial cell adhesion/activating molecule (EpCAM) expression in renal tumours: a retrospective clinicopathological study of 948 cases using tissue microarrays
Authors: Zimpfer Annette , Maruschke Matthias , Rehn Stefan , Kundt Guenter , Litzenberger Anke , Dammert Friederike , Zettl Heike , Stephan Carsten , Hakenberg Oliver W. , Erbersdobler Andreas 
Published: November 2013

Objective
To evaluate the expression and prognostic value of epithelial cell adhesion/activating molecule (EpCAM) in a large set of renal cell carcinomas (RCCs) using a tissue microarray (TMA) approach.
Material and Methods
We studied the immunohistochemical expression and overexpression of EpCAM on TMAs containing formalin‐fixed, paraffin‐embedded samples of 948 patients with documented renal tumours.
EpCAM expression was defined as the presence of a specific membranous staining in >5% of the tumour cells.
EpCAM overexpression was specified by calculating a total staining score (score range 0–12) as the product of a proportion score and an intensity score, and defined as a score >4.
Results
Of 948 cases, 927 (97.8%) were evaluable morphologically (haematoxylin and eosin stain). EpCAM expression was found in 233/642 (36.3%), 126/155 (81.3%), 54/68 (78.3%), 17/45 (37.8%), 13/30 (43.3%) of clear‐cell RCC, papillary RCC (pRCC), chromophobe RCC (cpRCC), oncocytomas and other unclassified tumour types, respectively.
Log‐rank tests showed a significantly longer overall survival (OS [P = 0.047]) and a trend of EpCAM expression to be associated with a longer progression‐free survival (PFS) in all RCC entities (P = 0.065).
EpCAM overexpression was significantly correlated with a better PFS in all RCC subtypes, cpRCC and pRCC (P = 0.011, 0.043 and 0.025, respectively).
In multivariate analysis EpCAM overexpression was an independent marker for longer PFS in all RCC entities as well as in high grade RCC (P = 0.009 and P = 0.010, respectively).
Conclusions
The histological subtypes associated with a high rate of EpCAM expression were cpRCC and pRCC.
This retrospective analysis demonstrated a trend towards longer OS and PFS for all major RCC subtypes.
EpCAM expression had significant prognostic value in patients with cpRCC and pRCC. Furthermore, EpCAM overexpression in high grade RCC may be a helpful marker for prognostication.
Recent insights into NF‐κB signalling pathways and the link between inflammation and prostate cancer
Authors: Nguyen Daniel P. , Li Jinyi , Yadav Shalini S. , Tewari Ashutosh K. 
Published: November 2013

Inflammation is involved in regulation of cellular events in prostate carcinogenesis through control of the tumour micro‐environment. A variety of bone marrow‐derived cells, including CD4+ lymphocytes, macrophages and myeloid‐derived suppressor cells, are integral components of the tumour micro‐environment.
On activation by inflammatory cytokines, NF‐κB complexes are capable of promoting tumour cell survival through anti‐apoptotic signalling in prostate cancer (PCa). Positive feedback loops are able to maintain NF‐κB activation.
NF‐κB activation is also associated with the metastatic phenotype and PCa progression to castration‐resistant prostate cancer (CRPC).
A novel role for inhibitor of NF‐κB kinase (IKK)‐α in NF‐κB‐independent PCa progression to metastasis and CRPC has recently been uncovered, providing a new mechanistic link between inflammation and PCa. Expansion of PCa progenitors by IKK‐α may be involved in this process.
In this review, we offer the latest evidence regarding the role of the NF‐κB pathway in PCa and discuss therapeutic attempts to target the NF‐κB pathways. We point out the need to further dissect inflammatory pathways in PCa in order to develop appropriate preventive measures and design novel therapeutic strategies.
The TRPA1 channel in migraine mechanism and treatment
Authors: Benemei S , Fusi C , Trevisan Gabriela , Geppetti Pierangelo 
Published: November 2013

Migraine remains an elusive and poorly understood disease. The uncertainty is reflected by the currently unsatisfactory acute and prophylactic treatments for this disease. Genetic and pharmacological information points to the involvement of some transient receptor potential (TRP) channels in pain mechanisms. In particular, the TRP vanilloid 1 (TRPV1) and TRP ankyrin 1 (TRPA1) channels seem to play a major role in different models of pain diseases. Recent findings have underscored the possibility that TRP channels expressed in the nerve terminals of peptidergic nociceptors contribute to the migraine mechanism. Among this channel subset, TRPA1, a sensor of oxidative, nitrative and electrophilic stress, is activated by an unprecedented series of irritant and pain‐provoking exogenous and endogenous agents, which release the pro‐migraine peptide, calcitonin gene‐related peptide, through this neuronal pathway. Some of the recently identified TRPA1 activators have long been known as migraine triggers. Furthermore, specific analgesic and antimigraine medicines have been shown to inhibit or desensitize TRPA1 channels. Thus, TRPA1 is emerging as a major contributing pathway in migraine and as a novel target for the development of drugs for pain and migraine treatment.Linked ArticlesThis article is part of a themed section on the pharmacology of TRP channels. To view the other articles in this section visit http://dx.doi.org/10.1111/bph.2014.171.issue‐10
Stoichiometry of δ subunit containing GABAA receptors
Authors: Patel B , Mortensen M , Smart T G 
Published: November 2013

Background and PurposeAlthough the stoichiometry of the major synaptic αβγ subunit‐containing GABAA receptors has consensus support for 2α:2β:1γ, a clear view of the stoichiometry of extrasynaptic receptors containing δ subunits has remained elusive. Here we examine the subunit stoichiometry of recombinant α4β3δ receptors using a reporter mutation and a functional electrophysiological approach.Experimental ApproachUsing site‐directed mutagenesis, we inserted a highly characterized 9′ serine to leucine mutation into the second transmembrane (M2) region of α4, β3 and δ subunits that increases receptor sensitivity to GABA. Whole‐cell, GABA‐activated currents were recorded from HEK‐293 cells co‐expressing different combinations of wild‐type (WT) and/or mutant α4(L297S), β3(L284S) and δ(L288S) subunits.Key ResultsRecombinant receptors containing one or more mutant subunits showed increased GABA sensitivity relative to WT receptors by approximately fourfold, independent of the subunit class (α, β or δ) carrying the mutation. GABA dose–response curves of cells co‐expressing WT subunits with their respective L9′S mutants exhibited multiple components, with the number of discernible components enabling a subunit stoichiometry of 2α, 2β and 1δ to be deduced for α4β3δ receptors. Varying the cDNA transfection ratio by 10‐fold had no significant effect on the number of incorporated δ subunits.Conclusions and ImplicationsSubunit stoichiometry is an important determinant of GABAA receptor function and pharmacology, and δ subunit‐containing receptors are important mediators of tonic inhibition in several brain regions. Here we demonstrate a preferred subunit stoichiometry for α4β3δ receptors of 2α, 2β and 1δ.
Drp1 is dispensable for apoptotic cytochrome c release in primed MCF10A and fibroblast cells but affects Bcl‐2 antagonist‐induced respiratory changes
Authors: Clerc P , Ge S X , Hwang H , Waddell J , Roelofs B A , Karbowski M , Sesaki H , Polster B M 
Published: November 2013

Background and PurposeDynamin‐related protein 1 (Drp1) mediates mitochondrial fission and is thought to promote Bax/Bak‐induced cytochrome c release during apoptosis. Conformationally active Bax, Bak and Bax/Bak‐activating BH3‐only proteins, such as Bim, are restrained by anti‐apoptotic Bcl‐2 proteins in cells that are ‘primed for death’. Inhibition of Bcl‐2/Bcl‐xL/Bcl‐w by the antagonist ABT‐737 causes rapid apoptosis of primed cells. Hence, we determined whether Drp1 is required for cytochrome c release, respiratory alterations and apoptosis of cells that are already primed for death.Experimental ApproachWe tested the Drp1 inhibitor mdivi‐1 for inhibition of cytochrome c release in MCF10A cells primed by Bcl‐2 overexpression. We measured ATP synthesis‐dependent, ‐independent and cytochrome c‐limited maximal oxygen consumption rates (OCRs) and cell death of immortalized wild‐type (WT) and Drp1 knockout (KO) mouse embryonic fibroblasts (MEFs) treated with ABT‐737.Key ResultsMdivi‐1 failed to attenuate ABT‐737‐induced cytochrome c release. ABT‐737 decreased maximal OCR measured in the presence of uncoupler in both WT and Drp1 KO MEF, consistent with respiratory impairment due to release of cytochrome c. However, Drp1 KO MEF were slightly less sensitive to this ABT‐737‐induced respiratory inhibition compared with WT, and were resistant to an initial ABT‐737‐induced increase in ATP synthesis‐independent O2 consumption. Nevertheless, caspase‐dependent cell death was not reduced. Pro‐apoptotic Bax was unaltered, whereas Bak was up‐regulated in Drp1 KO MEF.Conclusions and ImplicationsThe findings indicate that once fibroblast cells are primed for death, Drp1 is not required for apoptosis. However, Drp1 may contribute to ABT‐737‐induced respiratory changes and the kinetics of cytochrome c release.Linked ArticlesThis article is part of a themed issue on Mitochondrial Pharmacology: Energy, Injury & Beyond. To view the other articles in this issue visit http://dx.doi.org/10.1111/bph.2014.171.issue‐8
Reactive astrocytes and perivascular macrophages express NLRP3 inflammasome in active demyelinating lesions of multiple sclerosis and necrotic lesions of neuromyelitis optica and cerebral infarction
Authors: Kawana Natsuki , Yamamoto Yoji , Ishida Tsuyoshi , Saito Yuko , Konno Hidehiko , Arima Kunimasa , Satoh Jun‐ichi 
Published: November 2013

AbstractObjectiveInflammasome, activated by pathogen‐derived and host‐derived danger signals, constitutes a multimolecular signaling complex that serves as a platform for caspase‐1 (CASP1) activation and interleukin‐1β (IL‐1B) maturation. Mice deficient for NLRP3 inflammasome components are resistant to experimental autoimmune encephalomyelitis (EAE), suggesting a pro‐inflammatory role of NLRP3 inflammasome. However, at present, a pathological role of NLRP3 inflammasome in multiple sclerosis (MS) brains remains unknown.MethodsWe studied the expression of NLRP3 inflammasome components in active demyelinating lesions of MS by immunohistochemistry.ResultsReactive astrocytes and perivascular macrophages expressed all three components of NLRP3 inflammasome – NLRP3, ASC and CASP1 – along with IL‐1B in active demyelinating lesions of MS, active necrotic lesions of neuromyelitis optica (NMO) and acute necrotic lesions of cerebral infarction. In contrast, the levels of expression of NLRP3, ASC, CASP1, and IL‐1B were greatly reduced in chronic inactive lesions of MS and gliotic lesions of cerebral infarction. Furthermore, the great majority of ramified and amoeboid microglia did not express NLRP3 in active and inactive MS lesions.ConclusionsNLRP3 inflammasome could be activated chiefly in reactive astrocytes and infiltrating macrophages under the condition of active destruction of brain tissues that potentially provides a danger signal.