bluuebunny/crossref_metadata_2025_split huggingface dataset:
Negative wealth shock and short-term changes in depressive symptoms and medication adherence among late middle-aged adults
Authors: Pool Lindsay R , Needham Belinda L , Burgard Sarah A , Elliott Michael R , de Leon Carlos F Mendes 
Published: April 2017

BackgroundExperiencing a negative wealth shock in late middle age may cause high levels of stress and induce reductions in health-related consumption.MethodsWe used data on late middle age individuals (51–64 years) from the longitudinal US-based Health and Retirement Study (N=19 281) to examine the relationship between negative wealth shock and short-term outcomes that serve as markers of the pathways from wealth shock to health: elevated depressive symptoms, as a marker of the stress pathway and cost-related medication non-adherence (CRN), as a marker of the consumption pathway. Negative wealth shock was considered to be a loss of total net worth of 75% or more.ResultsUsing a nested cross-over approach—a within-person design among exposed individuals only that adjusts by design for all time-invariant individual characteristics—we found that negative wealth shock was significantly associated with increased odds of elevated depressive symptoms (OR=1.50, CI 1.10 to 2.05), but was not significantly associated with higher odds of CRN (OR=1.18, CI 0.76 to 1.82), even after further adjustment for time-varying sociodemographic and health covariates.ConclusionsNegative wealth shock during late middle age confers an increased risk of elevated depressive symptoms, but does not change levels of CRN. Personal and policy factors that may buffer the mental health risks of negative wealth shock, such as social support and social welfare policy, should be considered.
Chemotherapy-Resistant Human Acute Myeloid Leukemia Cells Are Not Enriched for Leukemic Stem Cells but Require Oxidative Metabolism
Authors: Farge Thomas , Saland Estelle , de Toni Fabienne , Aroua Nesrine , Hosseini Mohsen , Perry Robin , Bosc Claudie , Sugita Mayumi , Stuani Lucille , Fraisse Marine , Scotland Sarah , Larrue Clément , Boutzen Héléna , Féliu Virginie , Nicolau-Travers Marie-Laure , Cassant-Sourdy Stéphanie , Broin Nicolas , David Marion , Serhan Nizar , Sarry Audrey , Tavitian Suzanne , Kaoma Tony , Vallar Laurent , Iacovoni Jason , Linares Laetitia K. , Montersino Camille , Castellano Rémy , Griessinger Emmanuel , Collette Yves , Duchamp Olivier , Barreira Yara , Hirsch Pierre , Palama Tony , Gales Lara , Delhommeau François , Garmy-Susini Barbara H. , Portais Jean-Charles , Vergez François , Selak Mary , Danet-Desnoyers Gwenn , Carroll Martin , Récher Christian , Sarry Jean-Emmanuel 
Published: April 2017

Abstract
Chemotherapy-resistant human acute myeloid leukemia (AML) cells are thought to be enriched in quiescent immature leukemic stem cells (LSC). To validate this hypothesis in vivo, we developed a clinically relevant chemotherapeutic approach treating patient-derived xenografts (PDX) with cytarabine (AraC). AraC residual AML cells are enriched in neither immature, quiescent cells nor LSCs. Strikingly, AraC-resistant preexisting and persisting cells displayed high levels of reactive oxygen species, showed increased mitochondrial mass, and retained active polarized mitochondria, consistent with a high oxidative phosphorylation (OXPHOS) status. AraC residual cells exhibited increased fatty-acid oxidation, upregulated CD36 expression, and a high OXPHOS gene signature predictive for treatment response in PDX and patients with AML. High OXPHOS but not low OXPHOS human AML cell lines were chemoresistant in vivo. Targeting mitochondrial protein synthesis, electron transfer, or fatty-acid oxidation induced an energetic shift toward low OXPHOS and markedly enhanced antileukemic effects of AraC. Together, this study demonstrates that essential mitochondrial functions contribute to AraC resistance in AML and are a robust hallmark of AraC sensitivity and a promising therapeutic avenue to treat AML residual disease.
Significance: AraC-resistant AML cells exhibit metabolic features and gene signatures consistent with a high OXPHOS status. In these cells, targeting mitochondrial metabolism through the CD36–FAO–OXPHOS axis induces an energetic shift toward low OXPHOS and strongly enhanced antileukemic effects of AraC, offering a promising avenue to design new therapeutic strategies and fight AraC resistance in AML. Cancer Discov; 7(7); 716–35. ©2017 AACR.
See related commentary by Schimmer, p. 670.
This article is highlighted in the In This Issue feature, p. 653
The Influence of Atmospheric Cloud Radiative Effects on the Large-Scale Stratospheric Circulation
Authors: Li Ying , Thompson David W. J. , Huang Yi 
Published: April 2017

AbstractPrevious studies have explored the influence of atmospheric cloud radiative effects (ACRE) on the tropospheric circulation. Here the authors explore the influence of ACRE on the stratospheric circulation. The response of the stratospheric circulation to ACRE is assessed by comparing simulations run with and without ACRE. The stratospheric circulation response to ACRE is reproducible in a range of different GCMs and can be interpreted in the context of both a dynamically driven and a radiatively driven component.The dynamic component is linked to ACRE-induced changes in the vertical and meridional fluxes of wave activity. The ACRE-induced changes in the vertical flux of wave activity into the stratosphere are consistent with the ACRE-induced changes in tropospheric baroclinicity and thus the amplitude of midlatitude baroclinic eddies. They account for a strengthening of the Brewer–Dobson circulation, a cooling of the tropical lower stratosphere, a weakening and warming of the polar vortex, a reduction of static stability near the tropical tropopause transition layer, and a shortening of the time scale of extratropical stratospheric variability. The ACRE-induced changes in the equatorward flux of wave activity in the low-latitude stratosphere account for a strengthening of the zonal wind in the subtropical lower to midstratosphere.The radiative component is linked to ACRE-induced changes in the flux of longwave radiation into the lower stratosphere. The changes in radiative fluxes lead to a cooling of the extratropical lower stratosphere, changes in the static stability and cloud fraction near the extratropical tropopause, and a shortening of the time scales of extratropical stratospheric variability.The results highlight a previously overlooked pathway through which tropospheric climate influences the stratosphere.
A Method to Extrapolate the Diffuse Upwelling Radiance Attenuation Coefficient to the Surface as Applied to the Marine Optical Buoy (MOBY)
Authors: Voss Kenneth J. , Gordon Howard R. , Flora Stephanie , Johnson B. Carol , Yarbrough Mark , Feinholz Michael , Houlihan Terrence 
Published: April 2017

AbstractThe upwelling radiance attenuation coefficient KLu in the upper 10 m of the water column can be significantly influenced by inelastic scattering processes and thus will vary even with homogeneous water properties. The Marine Optical Buoy (MOBY), the primary vicarious calibration site for many ocean color sensors, makes measurements of the upwelling radiance Lu at 1, 5, and 9 m, and uses these values to determine KLu and to propagate the upwelling radiance directed toward the zenith, Lu, at 1 m to and through the surface. Inelastic scattering causes the KLu derived from the measurements to be an underestimate of the true KLu from 1 m to the surface at wavelengths greater than 575 nm; thus, the derived water-leaving radiance is underestimated at wavelengths longer than 575 nm. A method to correct this KLu, based on a model of the upwelling radiance including Raman scattering and chlorophyll fluorescence, has been developed that corrects this bias. The model has been experimentally validated, and this technique can be applied to the MOBY dataset to provide new, more accurate products at these wavelengths. When applied to a 4-month MOBY deployment, the corrected water-leaving radiance Lw can increase by 5% (600 nm), 10% (650 nm), and 50% (700 nm). This method will be used to provide additional and more accurate products in the MOBY dataset.
Corrective Nasal Surgery after Maxillomandibular Advancement for Obstructive Sleep Apnea: Experience from 379 Cases
Authors: Liu Stanley Yung‐Chuan , Lee Pi‐Jung , Awad Michael , Riley Robert W. , Zaghi Soroush 
Published: April 2017

ObjectiveEfficacy of maxillomandibular advancement (MMA) in the treatment of obstructive sleep apnea (OSA) is associated with degree of maxillary advancement. Large maxillary advancement leads to profound changes of the nasolabial region. We present the incidence and indications of post‐MMA corrective nasal surgery in a large cohort.Study DesignCase series with chart review.SettingUniversity medical center.Subjects and MethodsA total of 379 subjects with OSA underwent MMA at Stanford Hospital (surgeons: S.Y.L., R.W.R.) from August 1992 to December 2015. Data were collected on age, sex, American Society of Anesthesiologists score, polysomnography parameters, and history of nasal surgery. Primary outcome parameters were the incidence and indications of post‐MMA corrective nasal surgery.ResultsOf 379 subjects, the surgical success rate was 76.3% based on the change in respiratory disturbance index. Seventy‐one subjects (18.7%) underwent corrective nasal surgery after MMA, whereas 48 underwent functional nasal surgery and 23 underwent both functional and aesthetic nasal surgery. Lower oxygen saturation nadir and higher baseline respiratory disturbance index were associated with increased likelihood of post‐MMA corrective nasal surgery.ConclusionMMA surgical success is associated with degree of maxillary advancement, which is especially significant in patients with severe OSA. Patients must be counseled on its impact in nasal function and aesthetics. Our series, the largest to date to address this question, suggests that the incidence of post‐MMA corrective nasal surgery is at least 18.7%. Prospectively, refinement in MMA techniques is needed to minimize postoperative compromise in nasal form and function.
Is Neck Dissection Associated with an Increased Risk of Postoperative Stroke?
Authors: Cramer John D. , Patel Urjeet A. , Maas Matthew B. , Samant Sandeep , Smith Stephanie Shintani 
Published: April 2017

ObjectivePrior studies have reported widely disparate rates of postoperative stroke, with conflicting analyses of whether neck dissection is an independent risk factor.Study DesignCohort study.SettingAmerican College of Surgeons National Surgical Quality Improvement Program from 2005 to 2013.Subjects and MethodsWe compared the 30‐day rate of postoperative stroke between patients undergoing complete or modified radical neck dissection and a control cohort composed of those undergoing resections in the oral cavity, oropharynx, larynx, or hypopharynx without neck dissection. Propensity scores and paired statistics were used to compare the groups while adjusting for relevant covariates.ResultsWe identified 9697 patients, including 5827 with neck dissection and 3870 without neck dissection. In the full cohort, the rate of postoperative stroke was greater with neck dissection than without it (0.31% vs 0.11%, P =. 052), although the relationship was attenuated by propensity score matching to adjust for comorbidities (0.30% vs 0.13%, P =. 18). Among patients with ≥2 risk factors for carotid artery stenosis, neck dissection was associated with an increased rate of postoperative stroke (2.68% with bilateral neck dissection, 0.41% with unilateral neck dissection, and 0.24% without neck dissection, P =. 04). The incidence of stroke was strongly associated with 30‐day mortality (7.4% vs 0.2%, P <. 001).ConclusionsStroke is a rare but highly morbid complication after head and neck surgery. Compared with other head and neck surgery, neck dissection in patients at risk for carotid artery stenosis is associated with an increased risk of postoperative stroke.
Factors Influencing Cochlear Patency after Translabyrinthine Surgery
Authors: Rodgers Brian , Stucken Emily , Metrailer Aaron , Sargent Eric 
Published: April 2017

ObjectiveTo determine predictive factors for cochlear obliteration after translabyrinthine surgery for vestibular schwannoma.Study DesignCase series with chart review.SettingNeurotology referral center.Subjects and MethodsIn total, 345 charts were reviewed, resulting in 103 patients who underwent translabyrinthine surgery between January 2010 and July 2015 and had postoperative magnetic resonance imaging (MRI) for review. Surveillance MRI performed after translabyrinthine resection of vestibular schwannomas was reviewed. Heavily T2‐weighted MRI obtained an average of 21.8 months after surgery was reviewed to assess cochlear patency. Tumor size, preoperative audiograms, and MRI cochlear fluid‐attenuated inversion recovery (FLAIR) intensity were compared between patients with retained cochlear patency and those without.ResultsFifty‐four percent of patients retained cochlear patency after translabyrinthine surgery. Tumor size did not differ statistically between the 2 groups. There was no statistically significant difference in speech reception thresholds, pure‐tone average, or word recognition scores between patent and nonpatent groups. Preoperative MRI FLAIR intensity did not differ between groups.ConclusionsMore than half of patients retain cochlear patency after translabyrinthine vestibular schwannoma surgery. Cochlear patency is required for cochlear implant in patients with unilateral deafness. Preoperative tumor size, hearing performance, and intensity on MRI FLAIR do not predict cochlear patency. To prevent loss of opportunity for cochlear implantation, simultaneous implantation and cochlear lumen keeper placement are options.
Impact of cardiopulmonary bypass surgery on cytokines in epicardial adipose tissue: comparison with subcutaneous fat
Authors: Mach Lukas , Bedanova Helena , Soucek Miroslav , Karpisek Michal , Konecny Tomas , Nemec Petr , Orban Marek 
Published: April 2017

Background: Cardiac surgery and cardiopulmonary bypass (CPB) have been shown to stimulate a systemic inflammatory response which has been associated with adverse postoperative outcomes. Adipose tissue, both epicardial (EAT) and subcutaneous (SAT), is a known source of inflammatory cytokines, but its role in the pathophysiology of surgery- and CPB-induced systemic inflammatory response has not been fully elucidated. Therefore, we conducted a study to establish levels of selected cytokines in EAT and SAT prior to and after surgery with CPB. Methods: Adipose tissue samples were obtained from patients undergoing planned cardiac surgery on CPB. Samples from EAT and SAT were collected before and immediately after CPB. Levels of tumour necrosis factor-α (TNF-α), interleukin-6 (IL-6), adipocyte fatty acid-binding protein (AFABP), leptin and adiponectin were determined by ELISA, which were adjusted for a total concentration of proteins in the individual samples. Results: Samples from 77 patients (mean age 67.68 ± 11.5 years) were obtained and analysed. Leptin, adiponectin, TNF-α and AFABP were shown to decrease their concentrations statistically significantly in the EAT after CPB while no statistically significant drop was observed in the SAT. On the contrary, IL-6 showed only a slight and statistically insignificant decrease in the EAT after CPB and it was in the SAT where a statistically significant drop was observed. Discussion: One of the most relevant findings of this study was the marked decrease in EAT levels of TNF-α, AFABP, leptin and adiponectin after the CPB termination. Our results suggest that EAT might serve as a pool of cytokines which are released into the circulation in reaction to surgery with CPB. Should these novel findings be confirmed, new strategies to assess and possibly reduce EAT contribution on adverse outcomes of cardiac surgery may be developed.
Proximal femoral nail antirotation versus dynamic hip screw fixation for treatment of osteoporotic type 31-A1 intertrochanteric femoral fractures in elderly patients
Authors: Zeng Xianshang , Zhang Nan , Zeng Dan , Zhang Lili , Xu Ping , Cao Lei , Yu Weiguang , Zhan Ke , Zhang Xinchao 
Published: April 2017

Objective To evaluate long-term radiographic and functional outcomes between dynamic hip screw (DHS) and proximal femoral nail antirotation (PFNA) fixation for treatment of osteoporotic type 31-A1 intertrochanteric femoral fractures (IFFs) among elderly patients Methods A retrospective comparative study was carried out. Follow-up was performed at 1, 3, 6, 9, and 12 months postoperatively and yearly thereafter. The primary outcome was the radiographic outcome, and the secondary outcome was the functional outcome. Results A significant difference in radiographic complications was observed between the DHS group (n = 45, 40.2%) and PFNA group (n = 15, 13.6%). The risk of femoral shaft fracture after implant removal at the 1-year follow-up was increased by 0.9% (n = 1) and 6.3% (n = 7) in the PFNA and DHS groups, respectively. This difference persisted with rates of 3.6% (n = 4) and 12.5% (n = 14) at the final follow-up. Additionally, significant differences were present in the Harris hip score at each visit. Conclusion Our results indicate that PFNA yields better outcomes than DHS fixation among elderly patients with osteoporotic type 31-A1 IFFs.
Simultaneous Reconstruction of the Medial and Lateral Collateral Ligaments for Chronic Combined Ligament Injuries of the Ankle
Authors: Yasuda Toshito , Shima Hiroaki , Mori Katsunori , Tsujinaka Seiya , Neo Masashi 
Published: April 2017

Background: Objective data on chronic injuries of the medial collateral ligament (MCL) of the ankle are scarce. Chronic MCL injuries are frequently associated with lateral collateral ligament (LCL) injuries. For patients with chronic combined MCL and LCL injuries, the authors have performed simultaneous surgery of the 2 ligaments. Hypothesis: Simultaneous surgery of the 2 ligaments may be effectively used to treat chronic combined MCL and LCL injuries. Study Design: Case series; Level of evidence, 4. Methods: Surgical outcomes were evaluated in 29 consecutive patients presenting with chronic MCL and LCL injuries (30 ankles; 15 men and 14 women; mean age, 31 years; 13 competitive and 10 recreational athletes). Preoperative and postoperative clinical outcomes were measured with the Karlsson score and the Japanese Society for Surgery of the Foot (JSSF) ankle-hindfoot scale score. The patients underwent preoperative and postoperative functional measurements and a radiological examination. In addition, preoperative magnetic resonance imaging (MRI) results, arthroscopic findings, and histology of the MCL were evaluated. Results: Preoperatively, the deep fibers of the MCL did not appear striated in 29 ankles, and high-intensity signal changes were observed in 23 ankles on T2-weighted or gradient echo MRI. MCL ruptures were confirmed with arthroscopic surgery. Medial impingement lesions and focal chondral lesions were confirmed in 10 and 21 ankles, respectively. Histology of the reconstructed MCL showed dense collagen fibers with vessels. The mean postoperative follow-up period was 30 months (range, 24-52 months). There was a significant change between preoperative and postoperative Karlsson scores (69.0 vs 96.1 points, respectively; P < .0001) and JSSF scores (69.8 vs 94.5 points, respectively; P < .0001). On varus and valgus stress radiography, the postoperative talar tilt angle was significantly lower than the preoperative angle. Postoperative anterior displacement on stress radiography was significantly lower than preoperative anterior displacement. Postoperatively, all 23 athletes returned to their preinjury level of sports participation. Conclusion: MCL insufficiency resulted from medial ankle instability and medial impingement lesions. Outcomes in the patients indicated that MCL reconstruction or resection of medial impingement lesions, performed in addition to LCL reconstruction, is effective for treating chronic combined MCL and LCL injuries of the ankle.
HUS and atypical HUS
Authors: Jokiranta T. Sakari 
Published: April 2017

AbstractHemolytic uremic syndrome (HUS) is a thrombotic microangiopathy characterized by intravascular hemolysis, thrombocytopenia, and acute kidney failure. HUS is usually categorized as typical, caused by Shiga toxin–producing Escherichia coli (STEC) infection, as atypical HUS (aHUS), usually caused by uncontrolled complement activation, or as secondary HUS with a coexisting disease. In recent years, a general understanding of the pathogenetic mechanisms driving HUS has increased. Typical HUS (ie, STEC-HUS) follows a gastrointestinal infection with STEC, whereas aHUS is associated primarily with mutations or autoantibodies leading to dysregulated complement activation. Among the 30% to 50% of patients with HUS who have no detectable complement defect, some have either impaired diacylglycerol kinase ε (DGKε) activity, cobalamin C deficiency, or plasminogen deficiency. Some have secondary HUS with a coexisting disease or trigger such as autoimmunity, transplantation, cancer, infection, certain cytotoxic drugs, or pregnancy. The common pathogenetic features in STEC-HUS, aHUS, and secondary HUS are simultaneous damage to endothelial cells, intravascular hemolysis, and activation of platelets leading to a procoagulative state, formation of microthrombi, and tissue damage. In this review, the differences and similarities in the pathogenesis of STEC-HUS, aHUS, and secondary HUS are discussed. Common for the pathogenesis seems to be the vicious cycle of complement activation, endothelial cell damage, platelet activation, and thrombosis. This process can be stopped by therapeutic complement inhibition in most patients with aHUS, but usually not those with a DGKε mutation, and some patients with STEC-HUS or secondary HUS. Therefore, understanding the pathogenesis of the different forms of HUS may prove helpful in clinical practice.
Heparin-induced thrombocytopenia
Authors: Arepally Gowthami M. 
Published: April 2017

AbstractHeparin-induced thrombocytopenia (HIT) is an immune complication of heparin therapy caused by antibodies to complexes of platelet factor 4 (PF4) and heparin. Pathogenic antibodies to PF4/heparin bind and activate cellular FcγRIIA on platelets and monocytes to propagate a hypercoagulable state culminating in life-threatening thrombosis. It is now recognized that anti-PF4/heparin antibodies develop commonly after heparin exposure, but only a subset of sensitized patients progress to life-threatening complications of thrombocytopenia and thrombosis. Recent scientific developments have clarified mechanisms underlying PF4/heparin immunogenicity, disease susceptibility, and clinical manifestations of disease. Insights from clinical and laboratory findings have also been recently harnessed for disease prevention. This review will summarize our current understanding of HIT by reviewing pathogenesis, essential clinical and laboratory features, and management.
Immune dysfunctionality of replicative senescent mesenchymal stromal cells is corrected by IFNγ priming
Authors: Chinnadurai Raghavan , Rajan Devi , Ng Spencer , McCullough Kenneth , Arafat Dalia , Waller Edmund K. , Anderson Larry J. , Gibson Greg , Galipeau Jacques 
Published: April 2017

Key Points
Replication exhausted human MSCs display attenuated immunosuppressive properties partly because of defective kynurenine production. IFNγ prelicensing can rescue replicative senescence-associated immune defects of human bone marrow–derived MSCs.