bluuebunny/crossref_metadata_2025_split huggingface dataset:
Does schema therapy change schemas and symptoms? A systematic review across mental health disorders
Authors: Taylor Christopher D. J. , Bee Penny , Haddock Gillian 
Published: December 2016

PurposeSchema therapy was first applied to individuals with borderline personality disorder (BPD) over 20 years ago, and more recent work has suggested efficacy across a range of disorders. The present review aimed to systematically synthesize evidence for the efficacy and effectiveness of schema therapy in reducing early maladaptive schema (EMS) and improving symptoms as applied to a range of mental health disorders in adults including BPD, other personality disorders, eating disorders, anxiety disorders, and post‐traumatic stress disorder.MethodsStudies were identified through electronic searches (EMBASE, PsycINFO, MEDLINE from 1990 to January 2016).ResultsThe search produced 835 titles, of which 12 studies were found to meet inclusion criteria. A significant number of studies of schema therapy treatment were excluded as they failed to include a measure of schema change. The Clinical Trial Assessment Measure was used to rate the methodological quality of studies. Schema change and disorder‐specific symptom change was found in 11 of the 12 studies.ConclusionsSchema therapy has demonstrated initial significant results in terms of reducing EMS and improving symptoms for personality disorders, but formal mediation analytical studies are lacking and rigorous evidence for other mental health disorders is currently sparse.Practitioner points

First review to investigate whether schema therapy leads to reduced maladaptive schemas and symptoms across mental health disorders.

Limited evidence for schema change with schema therapy in borderline personality disorder (BPD), with only three studies conducting correlational analyses.

Evidence for schema and symptom change in other mental health disorders is sparse, and so use of schema therapy for disorders other than BPD should be based on service user/patient preference and clinical expertise and/or that the theoretical underpinnings of schema therapy justify the use of it therapeutically.

Further work is needed to develop the evidence base for schema therapy for other disorders.
Neuromuscular responses of the plantar flexors to whole‐body vibration
Authors: Harwood B. , Scherer J. , Brown R. E. , Cornett K. M. D. , Kenno K. A. , Jakobi J. M. 
Published: December 2016

Enhanced physical performance following whole‐body vibration (WBV) has been attributed to increased muscle activity; however, few studies have measured the mechanisms underlying these changes. The objective of this study was to measure the responsiveness of the Ia pathway as well as contractile properties in 16 young adults (24±2 years, eight men, eight women) following repeated bouts of acute WBV (45 Hz, 2 mm). Hoffman reflexes (H‐reflex), compound muscle action potentials (M‐wave), and twitch contractile properties were measured prior to and immediately following five 1‐minute WBV exposures, and at 3, 5, 10, and 20 minute post‐WBV. M‐wave and H‐reflex amplitudes decreased by 8% (P<.001) and by 46% (P<.05), respectively, whereas peak twitch torque decreased by 9% (P<.01) and rate of twitch torque development slowed 8% (P<.05). Percent voluntary activation and maximal plantar flexor torque were unchanged as a consequence of WBV (P>.05). In response to acute WBV, the root mean square of the soleus electromyography signal (EMGRMS) increased by 8%, while the EMGRMS of the lateral gastrocnemius increased by 3% (P<.05). These data indicate that the responsiveness of the Ia pathway is diminished and contractile function is impaired immediately following WBV, and that the neural mechanisms underlying improved performance following WBV lie in alternative hypotheses possibly involving spindle disfacilitation or Golgi afferent modulation.
The role of CD4 cell count as discriminatory measure to guide chemoprophylaxis against Pneumocystis jirovecii pneumonia in human immunodeficiency virus‐negative immunocompromised patients: A systematic review
Authors: Messiaen Peter E. , Cuyx Senne , Dejagere Tom , van der Hilst Jeroen C. 
Published: December 2016

AbstractBackgroundIn recent years, the incidence of Pneumocystis jirovecii pneumonia (PJP) has increased in immunocompromised patients without human immunodeficiency virus (HIV) infection. Chemoprophylaxis with trimethoprim‐sulfamethoxazole (TMP‐SMX) is highly effective in preventing PJP in both HIV‐positive and ‐seronegative patients. In HIV‐positive patients, the risk of PJP is strongly correlated with decreased CD4 cell count. The role of CD4 cell count in the pathogenesis of PJP in non‐HIV immunocompromised patients is less well studied. For most immunosuppressive conditions, no clear guidelines indicate whether to start TMP‐SMX.MethodWe conducted a systematic literature review with the aim to provide a comprehensive overview on the role of CD4 cell counts in managing the risk of PJP in HIV‐seronegative patients.ResultsOf the 63 individual studies retrieved, 14 studies report on CD4 cell counts in a variety of immunosuppressive conditions. CD4 cell count were <200/μL in 73.1% of the patients.ConclusionCD4 cell count <200/μL is a sensitive biomarker to identify non‐HIV immunocompromised patients who are at risk for PJP. Measuring CD4 cell counts could help clinicians identify patients who may benefit from TMP‐SMX prophylaxis.
Early diagnosis of Ehrlichia ewingii infection in a lung transplant recipient by peripheral blood smear
Authors: Regunath Hariharan , Rojas‐Moreno Christian , Olano Juan P. , Hammer Richard D. , Salzer William 
Published: December 2016

AbstractEhrlichiosis in lung transplant (LT) recipients is associated with severe outcomes. Ehrlichia ewingii is a less frequent cause of symptomatic ehrlichiosis, characterized by cytoplasmic inclusions (morulae) within circulating neutrophils. We report a case of E. ewingii infection in an LT recipient diagnosed promptly by blood smear exam and confirmed with molecular studies.
Additional intraarticular tranexamic acid further reduced postoperative blood loss compared to intravenous and topical bathed tranexamic acid in total hip arthroplasty: a retrospective sequential series study
Authors: Nakura Nariaki , Hirakawa Kazuo , Takayanagi Satoshi , Saito Akira , Tsuji Koji , Tamaki Yasunobu , Ochiai Shunsuke , Mihara Masahiko 
Published: December 2016

BACKGROUNDTopical tranexamic acid (TXA) administration has been described to be effective in decreasing blood loss in total hip arthroplasty (THA). The aim of this retrospective study was to evaluate whether topical intraarticular TXA administration in addition to intravenous (IV) and topical bathed TXA further reduces blood loss in THA patients.STUDY DESIGN AND METHODSFour‐hundred patients were enrolled in this sequential series study with two different phases during four different time periods. Patients were divided based on TXA usage and route of administration: those with and without IV TXA (IVTA‐I and no‐IVTA groups, respectively) and those with and without intraarticular TXA (TITA and IVTA‐II groups, respectively). Both IVTA‐II and TITA groups had IV TXA, and all four groups used topical bathed TXA. These four groups had 100 cases each. The primary outcomes were evaluated with total blood loss and postoperative hemoglobin level.RESULTSThe total blood loss was 1106 and 875 mL in the no‐IVTA and IVTA‐I groups, respectively (p < 0.05). Postoperative Hb was 10.9 and 11.51 g/dL in the no‐IVTA and IVTA‐I groups, respectively (p < 0.05). Total blood loss was 813 and 646 mL in the IVTA‐II and TITA groups, respectively (p < 0.05). Intraarticular with IV and bathed TXA administration was more effective than IV and bathed TXA in reducing blood loss.CONCLUSIONThis study suggests that the combined administration of topical intraarticular, bathed, and IV TXA was effective in reducing blood loss in THA patients.
Phylogeny and evolution of shallow‐water squat lobsters (Decapoda, Galatheoidea) from the Indo‐Pacific
Authors: Palero Ferran , Robainas‐Barcia Aymee , Corbari Laure , Macpherson Enrique 
Published: December 2016

Squat lobsters have a worldwide distribution and are highly visible crustaceans living in a broad range of habitats. In this study, partial sequences of two mitochondrialDNAgenes (16SrRNAandCOI) and a nuclear gene (H3) were obtained for all but one of the known species of the shallow‐water generaSadayoshia(Munididae) andLauriea,MacrotheaandTriodonthea(Galatheidae).Lauriea siagianiappeared to be phylogenetically closer toTriodontheaandMacrotheathan to otherLaurieaspecies, suggesting the need for taxonomic re‐evaluation of these taxa. All species ofSadayoshiaformed a monophyletic group that would have diverged during the Paleogene (around 50 Mya). Our results support the hypothesis that the late Paleogene–Neogene transition was a period of rapid diversification for shallow‐water species of both Galatheidae and Munididae in the Indo‐Pacific region. This is probably related to high tectonic activity among the Eurasian, Philippine Sea, Indo‐Australian and Pacific plates and corresponding changes in distribution of habitats and ocean currents during the late Paleogene. Finally, the tropical south‐west Pacific province is identified as a major diversification centre for shallow‐water squat lobsters, from where species dispersed to other Pacific and Indian Ocean regions.
Network properties of interstitial cells of Cajal affect intestinal pacemaker activity and motor patterns, according to a mathematical model of weakly coupled oscillators
Authors: Wei Ruihan , Parsons Sean P. , Huizinga Jan D. 
Published: December 2016

New Findings
What is the central question of this study?
What are the effects of interstitial cells of Cajal (ICC) network perturbations on intestinal pacemaker activity and motor patterns?

What is the main finding and its importance?
Two‐dimensional modelling of the ICC pacemaker activity according to a phase model of weakly coupled oscillators showed that network properties (coupling strength between oscillators, frequency gradient and frequency noise) strongly influence pacemaker network activity and subsequent motor patterns. The model explains motor patterns observed in physiological conditions and provides predictions and testable hypotheses for effects of ICC loss and frequency modulation on the motor patterns.

Interstitial cells of Cajal (ICC) are the pacemaker cells of gut motility and are associated with motility disorders. Interstitial cells of Cajal form a network, but the contributions of its network properties to gut physiology and dysfunction are poorly understood. We modelled an ICC network as a two‐dimensional network of weakly coupled oscillators with a frequency gradient and showed changes over time in video and graphical formats. Model parameters were obtained from slow‐wave‐driven contraction patterns in the mouse intestine and pacemaker slow‐wave activities from the cat intestine. Marked changes in propagating oscillation patterns (including changes from propagation to non‐propagating) were observed by changing network parameters (coupling strength between oscillators, the frequency gradient and frequency noise), which affected synchronization, propagation velocity and occurrence of dislocations (termination of an oscillation). Complete uncoupling of a circumferential ring of oscillators caused the proximal and distal section to desynchronize, but complete synchronization was maintained with only a single oscillator connecting the sections with high enough coupling. The network of oscillators could withstand loss; even with 40% of oscillators lost randomly within the network, significant synchronization and anterograde propagation remained. A local increase in pacemaker frequency diminished anterograde propagation; the effects were strongly dependent on location, frequency gradient and coupling strength. In summary, the model puts forth the hypothesis that fundamental changes in oscillation patterns (ICC slow‐wave activity or circular muscle contractions) can occur through physiological modulation of network properties. Strong evidence is provided to accept the ICC network as a system of coupled oscillators.
Genome Sequence of Actinomyces naeslundii Strain ATCC 27039, Isolated from an Abdominal Wound Abscess
Authors: Mashimo Chiho , Yamane Kazuyoshi , Yamanaka Takeshi , Maruyama Hugo , Wang Pao-Li , Komasa Satoshi , Okazaki Joji , Nambu Takayuki 
Published: December 2016

ABSTRACT

Here, we present the complete genome sequence of
Actinomyces naeslundii
strain ATCC 27039, isolated from an abdominal wound abscess. This strain is genetically transformable and will thus provide valuable information related to its crucial role in oral multispecies biofilm development.
Draft Whole-Genome Sequence of the Alkaliphilic Alishewanella aestuarii Strain HH-ZS, Isolated from Historical Lime Kiln Waste-Contaminated Soil
Authors: Salah Zohier B. , Rout Simon P. , Humphreys Paul N. 
Published: December 2016

ABSTRACT

Here, we present the whole-genome sequence of an environmental Gram-negative
Alishewanella aestuarii
strain (HH-ZS), isolated from the hyperalkaline contaminated soil of a historical lime kiln in Buxton, United Kingdom.
Ischemic preconditioning in pigs: a causal role for signal transducer and activator of transcription 3
Authors: Gent Sabine , Skyschally Andreas , Kleinbongard Petra , Heusch Gerd 
Published: December 2016

Ischemic preconditioning (IPC), i.e., brief episodes of nonlethal myocardial ischemia-reperfusion (I/R) before sustained ischemia with subsequent reperfusion, reduces infarct size in all species tested so far, including humans. In rodents, the cardioprotective signal transduction causally involves an activation of Akt, ERK1/2, and STAT3. However, there are apparent species differences in the signal transduction between rodents and larger mammals such as pigs, where data on IPC's signal transduction are inconsistent for Akt and ERK1/2. The role of STAT3 has not yet been analyzed. Pigs were subjected to 60 min of left anterior descending coronary artery occlusion and 180 min of reperfusion without or with IPC (2 cycles of 3-min occlusion separated by 2 min of reperfusion 15 min before sustained I/R). Infarct size was analyzed by triphenyl tetrazolium chloride staining, and Akt, ERK1/2, and STAT3 phosphorylation was quantified in myocardial biopsies taken at baseline and early reperfusion. AG490 was used to block the STAT3 signaling pathway. IPC reduced infarct size (%area at risk; mean ± SE, I/R, 45 ± 3 vs. IPC, 18 ± 3, P < 0.05). Akt and ERK1/2 phosphorylation was increased at early reperfusion without and with IPC. In contrast, STAT3 phosphorylation at early reperfusion was only increased with IPC (%baseline; mean ± SE, I/R, 126 ± 29 vs. IPC, 408 ± 147, P < 0.05). AG490 prevented the IPC-related increase of STAT3 phosphorylation at reperfusion (%baseline; mean ± SE, 82 ± 12) and abolished IPC's cardioprotection (%area at risk; mean ± SE, 35 ± 4). In pigs, increased phosphorylation of STAT3 is causally involved, whereas Akt and ERK1/2 seem to play no role in IPC's cardioprotection. NEW & NOTEWORTHY In pig hearts in situ, ischemic preconditioning (IPC) causally involves increased phosphorylation of STAT3, whereas Akt and ERK1/2 play no role for cardioprotection. The cardioprotective signal transduction of IPC is similar to that of ischemic postconditioning and remote IPC in pigs.
Polyclonal Secondary FGFR2 Mutations Drive Acquired Resistance to FGFR Inhibition in Patients with FGFR2 Fusion–Positive Cholangiocarcinoma
Authors: Goyal Lipika , Saha Supriya K. , Liu Leah Y. , Siravegna Giulia , Leshchiner Ignaty , Ahronian Leanne G. , Lennerz Jochen K. , Vu Phuong , Deshpande Vikram , Kambadakone Avinash , Mussolin Benedetta , Reyes Stephanie , Henderson Laura , Sun Jiaoyuan Elisabeth , Van Seventer Emily E. , Gurski Joseph M. , Baltschukat Sabrina , Schacher-Engstler Barbara , Barys Louise , Stamm Christelle , Furet Pascal , Ryan David P. , Stone James R. , Iafrate A. John , Getz Gad , Porta Diana Graus , Tiedt Ralph , Bardelli Alberto , Juric Dejan , Corcoran Ryan B. , Bardeesy Nabeel , Zhu Andrew X. 
Published: December 2016

Abstract
Genetic alterations in the fibroblast growth factor receptor (FGFR) pathway are promising therapeutic targets in many cancers, including intrahepatic cholangiocarcinoma (ICC). The FGFR inhibitor BGJ398 displayed encouraging efficacy in patients with FGFR2 fusion–positive ICC in a phase II trial, but the durability of response was limited in some patients. Here, we report the molecular basis for acquired resistance to BGJ398 in three patients via integrative genomic characterization of cell-free circulating tumor DNA (cfDNA), primary tumors, and metastases. Serial analysis of cfDNA demonstrated multiple recurrent point mutations in the FGFR2 kinase domain at progression. Accordingly, biopsy of post-progression lesions and rapid autopsy revealed marked inter- and intralesional heterogeneity, with different FGFR2 mutations in individual resistant clones. Molecular modeling and in vitro studies indicated that each mutation led to BGJ398 resistance and was surmountable by structurally distinct FGFR inhibitors. Thus, polyclonal secondary FGFR2 mutations represent an important clinical resistance mechanism that may guide the development of future therapeutic strategies.
Significance: We report the first genetic mechanisms of clinical acquired resistance to FGFR inhibition in patients with FGFR2 fusion–positive ICC. Our findings can inform future strategies for detecting resistance mechanisms and inducing more durable remissions in ICC and in the wide variety of cancers where the FGFR pathway is being explored as a therapeutic target. Cancer Discov; 7(3); 252–63. ©2016 AACR.
See related commentary by Smyth et al., p. 248.
This article is highlighted in the In This Issue feature, p. 235
Prothrombotic Fibrin Clot Phenotype Is Associated With Recurrent Pulmonary Embolism After Discontinuation of Anticoagulant Therapy
Authors: Zabczyk Michal , Plens Krzysztof , Wojtowicz Wioletta , Undas Anetta 
Published: December 2016

Objective—
Pulmonary embolism (PE) is a life-threatening manifestation of venous thromboembolism with a high recurrence rate after anticoagulation cessation. Recently, we have reported that prothrombotic clot phenotype in venous thromboembolism patients is associated with an increased risk of recurrent deep-vein thrombosis.

Approach and Results—

We tested whether abnormal clot properties are predictive of recurrent PE. We investigated 156 consecutive white patients aged 18 to 65 years after the first-ever provoked or unprovoked PE (n=89), with or without deep-vein thrombosis. Plasma fibrin clot permeability (K
s
), turbidity measurements, calibrated automated thrombography, and efficiency of fibrinolysis using clot lysis time, maximum D-dimer levels, and rate of increase in D-dimer levels were evaluated at ≥3 months of anticoagulant therapy, at least 4 weeks since the anticoagulation withdrawal. The primary end point was recurrent PE during a median follow-up of 50 months. Recurrent PE was diagnosed in 23 (14.7%; 5%/yr) patients. Recurrent PE was associated with formation of denser fibrin networks reflected by lower K
s
(
P
=0.007) and impaired fibrinolysis, as evidenced by prolonged clot lysis time (
P
=0.012) and reduced maximum rate of increase in D-dimer levels in the lysis assay (
P
=0.004). Patients with recurrent PE had higher plasma D-dimer (
P
<0.001) and thrombin peak (
P
=0.007) compared with the remainder, whereas turbidity measurements and maximum D-dimer levels did not differ in the recurrence. Multivariate model showed that independent predictors of recurrent PE were female sex, unprovoked venous thromboembolism, higher plasma D-dimer, reduced K
s
, and reduced maximum rate of increase in D-dimer levels in the lysis assay (all
P
<0.05).

Conclusions—
Altered fibrin clot properties including formation of more compact clots displaying impaired susceptibility to lysis may predispose to recurrent PE.
Role of KCa3.1 Channels in Macrophage Polarization and Its Relevance in Atherosclerotic Plaque Instability
Authors: Xu Rende , Li Chenguang , Wu Yizhe , Shen Li , Ma Jianying , Qian Juying , Ge Junbo 
Published: December 2016

Objective—
Emerging evidence indicates that proinflammatory macrophage polarization imbalance plays a key role in atherosclerotic plaque progression and instability. The calcium-activated potassium channel KCa3.1 is critically involved in macrophage activation and function. However, the role of KCa3.1 in macrophage polarization is unknown. This study investigates the potential role of KCa3.1 in transcriptional regulation in macrophage polarization and its relationship to plaque instability.

Approach and Results—
Human monocytes were differentiated into macrophages using macrophage colony-stimulating factor. Macrophages were then polarized into proinflammatory M1 cells by interferon-γ and lipopolysaccharide and into alternative M2 macrophages by interleukin-4. A model for plaque instability was induced by combined partial ligation of the left renal artery and left common carotid artery in apolipoprotein E knockout mice. Significant upregulation of KCa3.1 expression was observed during the differentiation of human monocytes into macrophages. Blocking KCa3.1 significantly reduced the expression of proinflammatory genes during macrophages polarization. Further mechanistic studies indicated that blocking KCa3.1 inhibited macrophage differentiation toward the M1 phenotype by downregulating signal transducer and activator of transcription-1 phosphorylation. In animal models, KCa3.1 blockade therapy strikingly reduced the incidence of plaque rupture and luminal thrombus in carotid arteries, decreased the expression of markers associated with M1 macrophage polarization, and enhanced the expression of M2 markers within atherosclerotic lesions.

Conclusions—
These results suggest that blocking KCa3.1 suppresses plaque instability in advanced stages of atherosclerosis by inhibiting macrophage polarization toward an M1 phenotype.
Protective Aptitude of Annexin A1 in Arterial Neointima Formation in Atherosclerosis-Prone Mice—Brief Report
Authors: de Jong Renske J. , Paulin Nicole , Lemnitzer Patricia , Viola Joana R. , Winter Carla , Ferraro Bartolo , Grommes Jochen , Weber Christian , Reutelingsperger Chris , Drechsler Maik , Soehnlein Oliver 
Published: December 2016

Objective—
Restenosis as a consequence of arterial injury is aggravated by inflammatory pathways. Here, we investigate the role of the proresolving protein annexin A1 (AnxA1) in healing after wire injury.

Approach and Results—

Apoe
−/−
and
Apoe
−/−
Anxa1
−/−
mice were subjected to wire injury while fed a high-cholesterol diet. Subsequently, localization of AnxA1 and AnxA1 plasma levels were examined. AnxA1 was found to localize within endothelial cells and macrophages in the neointima. Levels of AnxA1 in the plasma and its lesional expression negatively correlated with neointima size, and in the absence of AnxA1, neointima formation was aggravated by the accumulation and proliferation of macrophages. In contrast, reendothelialization and smooth muscle cell infiltration were not affected in
Apoe
−/−
Anxa1
−/−
mice.

Conclusions—
AnxA1 is protective in healing after wire injury and could, therefore, be an attractive therapeutic compound to prevent from restenosis after vascular damage.