bluuebunny/crossref_metadata_2025_split huggingface dataset:
γ-Aminobutyric Acid Receptor Type A Receptor Potentiation Reduces Firing of Neuronal Assemblies in a Computational Cortical Model
Authors: Storer Kingsley P. , Reeke George N. 
Published: August 2012

Background
The understanding of how general anesthetics act on individual cells and on global brain function has increased significantly during the last decade. What remains poorly understood is how anesthetics act at intermediate scales. Several major theories emphasize the importance of neuronal groups, sets of strongly connected neurons that fire in a time-locked fashion, in all aspects of brain function, particularly as a necessary substrate of consciousness. The authors have undertaken computer modeling to determine how ã-aminobutyric acid receptor type A (GABAA) receptor potentiating agents such as propofol may influence the dynamics of neuronal group formation and ongoing activity.

Methods
A computer model of a cortical network with connections modified by synaptic plasticity was examined. At baseline, the model spontaneously formed neuronal groups. Direct effects of GABAA receptor potentiation and indirect effects on input drive were then examined to study their effects on this process.

Results
Potentiation of GABAA inhibition and input drive reduction reduced the firing frequency of inhibitory and excitatory neurons in a dose-dependent manner. The diminution in spiking rates led to dramatic reductions in the firing frequency of neuronal groups. Simulated electroencephalographic output from the model at baseline exhibits gamma and theta rhythmicity. The direct and indirect GABAA effects reduce the amplitude of these underlying rhythms and modestly slow the gamma rhythm.

Conclusions
GABAA facilitation both directly and indirectly inhibits the ability of neurons to form groups spontaneously. A lack of group formation is consistent with some theories of anesthetic-induced loss of memory formation and consciousness.
Deficits in Retention for Verbally Presented Medical Information
Authors: Sandberg Elisabeth H. , Sharma Ritu , Sandberg Warren S. 
Published: August 2012

Background
Anesthesiologists deliver large quantities of verbal information to patients during preoperative teaching. Basic principles of cognitive psychology dictate that much of this information is likely to be forgotten. Exactly how much and what type of information can be retained and recalled remains an open question.

Methods
With Institutional Review Board approval, 98 healthy, educated volunteers viewed a brief video containing a preoperative explanation of anesthetic options and instructions. Subjects were then asked to engage in free and cued recall of information from the video, and to complete a recognition task. We developed a coding scheme to objectively score the free and cued recall tasks for the quantity of information recalled relative to the quantity presented in the video. Data are presented as descriptive statistics.

Results
Subjects spontaneously recalled less than 25% of the information presented. Providing retrieval cues greatly enhanced recall: Subjects recalled 67%, on average, of the material queried in the cued recall task. Performance was even stronger on the multiple-choice test (83% of items correctly answered), indicating that the information was initially encoded. The category of information that was consistently least-remembered was presurgical medication instructions.

Conclusions
Under realistic conditions for recall, most medical instruction given to patients will not be recalled, even if it is initially encoded. Given the limits of short-term memory, clinicians should carefully consider their patterns of information giving. Improvement of memory performance with cues for retrieval indicates that providing printed instructions for later review may be beneficial.
Epinephrine Induces Rapid Deterioration in Pulmonary Oxygen Exchange in Intact, Anesthetized Rats
Authors: Krishnamoorthy Vijay , Hiller David B. , Ripper Richard , Lin Bocheng , Vogel Stephen M. , Feinstein Douglas L. , Oswald Sarah , Rothschild Leelach , Hensel Priscilla , Rubinstein Israel , Minshall Richard , Weinberg Guy L. 
Published: August 2012

Background
Previous studies indicate epinephrine adversely affects arterial oxygenation when administered in a rat model of local anesthetic overdose. The authors tested whether epinephrine alone exerts similar effects in the intact animal.

Methods
Anesthetized rats received a single intravenous injection of epinephrine (25, 50, or 100 mcg/kg); matched cohorts were pretreated with phentolamine (100 mcg/kg); n = 5 for each of the six treatment groups. Arterial pressure and blood gases were measured at baseline, 1 and 10 min after epinephrine administration. Pulmonary capillary pressures during epinephrine infusion with normal and increased flows were measured in an isolated lung preparation.

Results
Epinephrine injection in the intact animal caused hypoxemia, hypercapnia, and acidosis at all doses. Arterial oxygen tension was reduced within 1 min of injection. Hyperlactatemia occurred by 10 min after 50 and 100 mcg/kg. Rate pressure product was decreased by 10 min after 100 mcg/kg epinephrine. Pretreatment with phentolamine attenuated these effects except at 100 mcg/kg epinephrine. In the isolated lung preparation, epinephrine in combination with increased pulmonary flow increased pulmonary capillary pressure and lung water.

Conclusions
Bolus injection of epinephrine in the intact, anesthetized rat impairs pulmonary oxygen exchange within 1 min of treatment. Effects were blunted by α-adrenergic receptor blockade. Edema occurred in the isolated lung above a threshold pulmonary capillary pressure when epinephrine treatment was coupled with an increase in pulmonary flow. These results potentially argue against using traditional doses of epinephrine for resuscitation, particularly in the anesthetized patient.
The Effector SPRYSEC-19 ofGlobodera rostochiensisSuppresses CC-NB-LRR-Mediated Disease Resistance in Plants
Authors: Postma Wiebe J. , Slootweg Erik J. , Rehman Sajid , Finkers-Tomczak Anna , Tytgat Tom O.G. , van Gelderen Kasper , Lozano-Torres Jose L. , Roosien Jan , Pomp Rikus , van Schaik Casper , Bakker Jaap , Goverse Aska , Smant Geert 
Published: August 2012

AbstractThe potato cyst nematode Globodera rostochiensis invades roots of host plants where it transforms cells near the vascular cylinder into a permanent feeding site. The host cell modifications are most likely induced by a complex mixture of proteins in the stylet secretions of the nematodes. Resistance to nematodes conferred by nucleotide-binding-leucine-rich repeat (NB-LRR) proteins usually results in a programmed cell death in and around the feeding site, and is most likely triggered by the recognition of effectors in stylet secretions. However, the actual role of these secretions in the activation and suppression of effector-triggered immunity is largely unknown. Here we demonstrate that the effector SPRYSEC-19 of G. rostochiensis physically associates in planta with the LRR domain of a member of the SW5 resistance gene cluster in tomato (Lycopersicon esculentum). Unexpectedly, this interaction did not trigger defense-related programmed cell death and resistance to G. rostochiensis. By contrast, agroinfiltration assays showed that the coexpression of SPRYSEC-19 in leaves of Nicotiana benthamiana suppresses programmed cell death mediated by several coiled-coil (CC)-NB-LRR immune receptors. Furthermore, SPRYSEC-19 abrogated resistance to Potato virus X mediated by the CC-NB-LRR resistance protein Rx1, and resistance to Verticillium dahliae mediated by an unidentified resistance in potato (Solanum tuberosum). The suppression of cell death and disease resistance did not require a physical association of SPRYSEC-19 and the LRR domains of the CC-NB-LRR resistance proteins. Altogether, our data demonstrated that potato cyst nematodes secrete effectors that enable the suppression of programmed cell death and disease resistance mediated by several CC-NB-LRR proteins in plants.
Single‐nucleotide variants in two Hedgehog genes, SHH and HHIP, as genetic cause of combined pituitary hormone deficiency
Authors: Blanco Darya Gorbenko del , de Graaff Laura C. G. , Visser Theo J. , Hokken‐Koelega Anita C. S. 
Published: August 2012

SummaryObjectiveCombined pituitary hormone deficiency (CPHD) is characterized by deficiencies of two or more anterior pituitary hormones. Its genetic cause is unknown in the majority of cases. The Hedgehog (Hh) signalling pathway has been implicated in disorders associated with pituitary development. Mutations in Sonic Hedgehog (SHH) have been described in patients with holoprosencephaly (with or without pituitary involvement). Hedgehog interacting protein (HHIP) has been associated with variations in adult height in genome wide association studies. We investigated whether mutations in these two genes of the Hh pathway, SHH and HHIP, could result in ′idiopathic′ CPHD.Design/PatientsWe directly sequenced the coding regions and exon – intron boundaries of SHH and HHIP in 93 CPHD patients of the Dutch HYPOPIT study in whom mutations in the classical CPHD genes PROP1, POU1F1, HESX1, LHX3 and LHX4 had been ruled out. We compared the expression of Hh genes in Hep3B transfected cells between wild‐type proteins and mutants.ResultsWe identified three single‐nucleotide variants (p.Ala226Thr, c.1078C>T and c.*8G>T) in SHH. The function of the latter was severely affected in our in vitro assay. In HHIP, we detected a new activating variant c.‐1G>C, which increases HHIP's inhibiting function on the Hh pathway.ConclusionsOur results suggest involvement of the Hedgehog pathway in CPHD. We suggest that both SHH and HHIP are investigated as a second screening in CPHD, after mutations in the classical CPHD genes have been ruled out.
Association of sex steroids, gonadotrophins, and their trajectories with clinical cardiovascular disease and all‐cause mortality in elderly men from the Framingham Heart Study
Authors: Haring Robin , Teng Zhaoyang , Xanthakis Vanessa , Coviello Andrea , Sullivan Lisa , Bhasin Shalender , Murabito Joanne M. , Wallaschofski Henri , Vasan Ramachandran S. 
Published: August 2012

SummaryBackgroundEmerging data from longitudinal studies suggest that low sex steroid concentrations in men are associated with increased cardiovascular risk and mortality. The impact of longitudinal trajectory patterns from serial sex steroid and gonadotrophin measurements on the observed associations is unknown to date.MethodsWe prospectively evaluated 254 elderly men (mean age, 75·5 years) of the Framingham Heart Study with up to four serial measurements of serum total testosterone (TT), dehydroepiandrosterone sulphate (DHEAS), follicle‐stimulating hormone (FSH), luteinizing hormone (LH) and total estradiol (EST); and constructed age‐ and multivariable‐adjusted Cox proportional hazard regression models relating baseline hormone concentrations and their mean, slope and variation over time (modelled as continuous and categorized into quartiles) to the incidence of clinical cardiovascular disease (CVD) and all‐cause mortality at 5‐ and 10‐year follow‐up.ResultsWe observed no association between baseline concentrations of sex steroids, gonadotrophins and their trajectories with incident clinical CVD over 5‐ and 10‐year follow‐up. Although higher baseline TT concentrations were associated with lower mortality risk at 5 years (hazard ratio per quartile increment, 0·74; 95% confidence interval, 0·56–0·98), correction for multiple statistical testing (P < 0·005) rendered this association statistically nonsignificant. Repeat analyses at the 10‐year follow‐up time point also demonstrated no significant association between sex steroids, gonadotrophins or their trajectories and mortality.ConclusionInvestigating longitudinal trajectory patterns of serial sex steroid and gonadotrophin measurements, the present study found no consistent associations with incident clinical CVD and all‐cause mortality risk in elderly men from the community.
Plasma YKL‐40 predicts 10‐year cardiovascular and all‐cause mortality in individuals with type 2 diabetes
Authors: Lin Chih‐Hung , Li Hung‐Yuan , Jiang Yi‐Der , Chang Tien‐Jyun , Chuang Lee‐Ming 
Published: August 2012

SummaryObjectiveElevated YKL‐40 concentrations have been observed in both coronary heart disease (CHD) and diabetes. Thus, YKL‐40 may play a role in pathogenesis of CHD in patients with diabetes. We evaluated whether plasma YKL‐40 concentration can predict all‐cause and cardiovascular mortality in individuals with type 2 diabetes.DesignThis is a prospective, observational study.PatientsA total of 628 subjects with type 2 diabetes were recruited between July 1996 and June 2003.MeasurementsPlasma YKL‐40 concentrations were measured via enzyme‐linked immunosorbent assay (ELISA). The cohort was followed up until 31 December 2008, when vital status and causes of death were obtained. Survival analysis and concordance statistics were performed. All‐cause and cardiovascular mortalities were documented.ResultsThere were 153 (24·36%) mortalities, including 48 participants (7·64%) who died from cardiovascular diseases (CVDs). Participants with higher plasma YKL‐40 (defined with a level above the median of 87·5 μg/l) had an increased risk of mortality. After adjusting for confounding variables, the hazard ratios (HR) for all‐cause and cardiovascular mortality in participants with higher plasma YKL‐40 were 1·97 (95% CI, 1·31–2·95, P < 0·01) and 2·45 (95% CI, 1·11–5·37, P < 0·05). The results remained similar after adjustment for age. Concordance statistics revealed that plasma YKL‐40 concentration significantly increases the predictive power for both all‐cause and cardiovascular mortality in different models.ConclusionsPlasma YKL‐40 concentration is an independent predictor of 10‐year all‐cause and cardiovascular mortality in subjects with type 2 diabetes. Further investigations on the role of YKL‐40 in the pathogenesis of CVD are required to elucidate the underlying mechanisms.
Thigh muscle attenuation measured by computed tomography was associated with the risk of low bone density in community‐dwelling elderly population
Authors: Kim Jung Hee , Choi Sung Hee , Lim Soo , Lim Jae Young , Kim Ki Woong , Park Kyong Soo , Shin Chan Soo , Jang Hak Chul 
Published: August 2012

SummaryObjectivesAlthough muscle mass has been shown to be positively related with bone mineral density (BMD), there are only a few studies that investigated the association between muscle strength or muscle quality and BMD. We investigated the effects of muscle strength and muscle fat infiltration, as a measure of muscle quality, adjusted for muscle mass on femoral neck BMD in Korean elderly cohort.MethodsWe recruited 242 men and 231 women aged over 65 years who participated in the Korean Longitudinal Study on Health and Ageing. Leg muscle mass and femoral neck BMD were measured by dual‐energy X‐ray absorptiometry. Isokinetic strength of knee extensors was measured as a peak torque value by an isokinetic device. Computed tomography scan of the mid‐thigh measured the mean Hounsfield unit (HU) of the lean tissue. Low bone density was defined as femoral neck T‐score ≤−2·0.ResultsLeg muscle mass, knee extensor strength and thigh muscle HU values were significantly positively correlated with femoral neck BMD in both men and women. However, muscle strength was not a significant determinant for the presence of low bone mass after adjusting for muscle mass in multiple logistic regression analyses. Notably, thigh muscle HU values were strong and independent determinant for the risk of low bone density.ConclusionDecreased thigh muscle HU values, a measure of fatty infiltration of muscle, were independently associated with increased risk of low bone density in the elderly population.
An audit of growth hormone replacement for GH‐deficient adults in Scotland
Authors: Philip Sam , Howat Isobel , Carson Maggie , Booth Anne , Campbell Karen , Grant Donna , Patterson Catherine , Schofield Christopher , Bevan John , Patrick Alan , Leese Graham , Connell John 
Published: August 2012

SummaryObjectiveGuidelines on the clinical use of growth hormone therapy in adults were issued by the UK National Institute for Clinical Excellence (NICE) in August 2003. We conducted a retrospective clinical audit on the use of growth hormone (GH) in Scotland to evaluate the use of these guidelines and their impact on clinical practice. The audit had two phases. In phase I, the impact of NICE criteria on specialist endocrine practice in starting and continuing GH replacement was assessed. In phase II, the reasons why some adults in Scotland with growth hormone deficiency were not on replacement therapy were evaluated.MethodsA retrospective cross‐sectional case note review was carried out of all adult patients being followed up for growth hormone deficiency during the study period (1 March 2005 to 31 March 2008). Phase I of the audit included 208 patients and phase II 108 patients.ResultsSellar tumours were the main cause of GH deficiency in both phases of the audit. In phase I, 53 patients (77%) had an AGHDA‐QoL score >11 documented before commencing GH post‐NICE guidance, compared with 35 (25%) pre‐NICE guidance. Overall, only 39 patients (18%) met the full NICE criteria for starting and continuing GH (pre‐NICE, 11%; post‐NICE, 35%). Phase II indicated that the main reasons for not starting GH included perceived satisfactory quality of life (n = 47, 43%), patient reluctance (16, 15%) or a medical contraindication (16, 15%).ConclusionsAlthough the use of quality of life assessments has increased following publication of the NICE guidelines, most adults on GH in Scotland did not fulfil the complete set of NICE criteria. The main reason for not starting GH therapy in adult GH‐deficient patients was perceived satisfactory quality of life.
Transposition of the miniature inverted‐repeat transposable element mimp1 in the wheat pathogen Fusarium culmorum
Authors: Spanu Francesca , Pasquali Matias , Scherm Barbara , Balmas Virgilio , Marcello Angela , Ortu Giuseppe , Dufresne Marie , Hoffmann Lucien , Daboussi Marie‐Josée , Migheli Quirico 
Published: August 2012

SummaryHigh‐throughput methods are needed for functional genomics analysis in Fusarium culmorum, the cause of crown and foot rot on wheat and a type B trichothecene producer. Our aim was to develop and test the efficacy of a double‐component system based on the ability of the impala transposase to transactivate the miniature inverted‐repeat transposable element mimp1 of Fusarium oxysporum. We report, for the first time, the application of a tagging system based on a heterologous transposon and of splinkerette‐polymerase chain reaction to identify mimp1 flanking regions in the filamentous fungus F. culmorum. Similar to previous observations in Fusarium graminearum, mimp1 transposes in F. culmorum by a cut‐and‐paste mechanism into TA dinucleotides, which are duplicated on insertion. mimp1 was reinserted in open reading frames in 16.4% (i.e. 10 of 61) of the strains analysed, probably spanning throughout the entire genome of F. culmorum. The effectiveness of the mimp1/impala double‐component system for gene tagging in F. culmorum was confirmed phenotypically for a putative aurofusarin gene. This system also allowed the identification of two genes putatively involved in oxidative stress‐coping capabilities in F. culmorum, as well as a sequence specific to this fungus, thus suggesting the valuable exploratory role of this tool.
Balancing conservation and recreational fishery objectives for a threatened fish species, the Murray cod, Maccullochella peelii
Authors: Koehn J. D. , Todd C. R. 
Published: August 2012

AbstractMurray cod Maccullochella peelii (Mitchell) is a large, iconic Australian fish species targeted by anglers but also listed as nationally threatened. A consultative process that included conservation and fishery interests helped to develop a population model for this species and agree on management scenarios to be tested. The modelled scenarios illustrated that threats to populations (risk of decline) can be substantially reduced and catch rates increased through harvest slot length limits (HSLL) rather than minimum legal limits (MLL). A 600‐ to 1000‐mm HSLL provided lower risk of decline and greater catch rates than the existing 500‐mm MLL, but better results were achieved with a 400‐ to 600‐mm HSLL. Importantly, a range of other impacts (fish kills, stocking, thermal impacts, larval mortalities, habitat changes) were recognised and incorporated. This study provides an example of the utility of a population model to improve management decision‐making for both conservation and fishery objectives.
How to increase activity level in the acute phase after stroke
Authors: van de Port Ingrid GL , Valkenet Karin , Schuurmans Marieke , Visser‐Meily Johanna MA 
Published: August 2012

Aims and objectives.  To study how patients with acute stroke spend their day and to determine whether activity levels of patients with acute stroke in a Dutch university hospital increase after the implementation of interventions to stimulate activity.Background.  Previous studies suggest that patients with acute stroke are prone to inactivity. Early mobilisation and increasing levels of activities are part of several guidelines for patients with stroke. However, implementing interventions to increase activity levels is difficult owing to time and money constrains.Design.  This study used a descriptive pre/postdesign.Methods.  Outcomes is assessed on three levels: location, other people involved and activity, and it is determined by direct non‐participant observation. An intervention was implemented to stimulate activity levels of the patients. This intervention consisted of (1) increasing the group therapy session and (2) providing a therapy guide that includes exercises patients can do by themselves or together with nurses, therapists or their family to stimulate the patients to be more active.Results.  In total, 66 patients have been observed: 35 during the first and 31 during the second observation periods. Compared with the first observation period, patients in the second observation period spent less time in their room and spent less time lying in bed (49 vs. 29%). They did spend more time sitting in bed (13% vs. 20%) and sitting supported (14% vs. 24%).Conclusion.  Simple interventions can lead to less inactivity in patients with acute stroke. Nurses should be highly involved in implementing and stimulating these interventions. Also, family can play an important role in reducing inactivity in patients after stroke.Relevance to clinical practice.  Nurses can play an important role in increasing activity levels of patients by using simple interventions.
My Brain Made Me Do It, and My Gut Didn’t Help
Authors: Menzies John 
Published: August 2012

SummaryDecisions about what, when and how much to eat are made by the brain, though these choices can be strongly influenced by the hedonic and rewarding properties of sweet or fatty foods. The rumbling before and the fullness after eating tells us that the gut also has an important role in the initiation and termination of feeding. Gut‐derived peptides continually convey homeostatic information to the brain to guide feeding. These circulating signals can also modify the pleasure and reward associated with food.