bluuebunny/crossref_metadata_2025_split huggingface dataset:
Preoperative anemia increases the risk of red blood cell transfusion and prolonged hospital length of stay in children undergoing spine arthrodesis surgery
Authors: Fontanals Montserrat , O'Leary James D. , Zaarour Christian , Skelton Teresa , Faraoni David 
Published: November 2018

BACKGROUNDPreoperative anemia is an important modifiable risk factor for red blood cell (RBC) transfusion in a variety of surgical populations. The primary objective of this study was to examine the association between preoperative anemia and i) transfusion of RBCs within 72 hours of surgery and ii) postoperative clinical outcomes in children undergoing spine arthrodesis surgery.STUDY DESIGN AND METHODSWe assembled a retrospective cohort of children included in the American College of Surgeons National Quality Improvement Program Pediatric database who underwent spine arthrodesis surgery from 2012 to 2016. Anemia was defined using age‐ and sex‐specific hematocrit thresholds. Data collected included demographic and surgical characteristics, RBC transfusion within 72 hours, and 30‐day postoperative outcomes (postoperative mechanical ventilation, infection, readmission, hospital length of stay, mortality). Multivariable logistic regression analyses were used to identify independent predictors of RBC transfusion and postoperative outcomes.RESULTSWe included 9,095 patients in the analysis. Preoperative anemia was present in 14% (n = 1,233) of the population and 67% (n = 6,135) of patients were transfused. Our multivariable logistic regression showed anemia, surgical time > 350 minutes, > 7 vertebral levels fused, neuromuscular disease, and cerebral palsy were all independent predictors of RBC transfusion. Preoperative anemia was also associated with prolonged hospital LOS (adjusted OR: 1.31, 95%CI: 1.11–1.54, p = 0.002).CONCLUSIONSIn this study of 9,095 children undergoing spine surgery, preoperative anemia was associated with an increased risk of RBC transfusion and prolonged LOS. Further studies are needed to determine if treatment of preoperative anemia can effectively reduce intraoperative RBC transfusion.
Serum amyloid A concentration in postoperative colic horses and its association with postoperative complications
Authors: Aitken Maia R. , Stefanovski Darko , Southwood Louise L. 
Published: November 2018

AbstractObjectiveTo determine serum amyloid A (SAA) concentrations in the postoperative (PO) colic horse and its association with PO complications and infection.Study designProspective case series.AnimalsFifty‐one horses after colic surgery.MethodsBlood samples from horses undergoing exploratory celiotomy were analyzed for quantitative SAA and fibrinogen concentrations and for neutrophil count at days 0, 1, 2, and 4‐6 and at hospital discharge.ResultsComplications developed in 35 (69%) horses and included PO colic (n = 13, 25%), PO reflux (n = 11, 22%), intravenous catheter (IVC) complications (n = 11, 22%), low‐grade fever (n = 11, 22%); surgical site infection (SSI; n = 9, 18%), high‐grade fever (n = 7, 14%), and diarrhea (n = 4, 8%). There was an association between day 2 SAA and PO colic (P = .004), diarrhea (P = .042), IVC complications (P = .008), and PO reflux (P = .008) as well as day 4‐6 SAA and PO colic (P = .004) and diarrhea (P = .018). Discharge SAA concentration was associated with SSI (P = .001). Fibrinogen concentrations at days 4‐6 and at discharge were associated with PO colic (P = .003), diarrhea (P = .004), IVC complications (P = .002), and PO reflux (P = .023). No differences were seen in SAA, fibrinogen, or neutrophils between horses with PO infection vs those with non–infection‐associated complications.ConclusionSerum amyloid A was markedly increased in the PO period in all horses but did not differ between PO infection and noninfection complications. The amount of inflammation associated with PO colic and colic surgery was high and may have affected the predictive value of SAA for early PO infection.Clinical significanceAlthough increases occurred earlier, measurement of SAA with a point‐of‐care analyzer may not be a more sensitive indicator of infection in the early PO colic horse than fibrinogen concentration. Serum amyloid A may help detect SSI in the late PO period.
Transformation of health professional/patient caring relationships through information and communication technologies used in telemedicine: a scoping review protocol
Authors: Thorup Charlotte Brun , Bundgaard Karin , Pedersen Preben U. 
Published: November 2018

Review objectives/questions
The objectives of this scoping review are to examine and map how telemedicine via information and communication technology (ICT) transforms caring relationships between health professionals and patients and how this transformation is conceptualized.
The questions of this review are:
La cooperación sur-sur de Brasil y Colombia: entre la política exterior y el desarrollo
Authors: Ruiz Camacho Paula Ximena 
Published: November 2018

La cooperación Sur-Sur es una modalidad complementaria a la tradicional cooperación Norte-Sur, la cual se ha fortalecido a lo largo de este siglo como un instrumento de soft power ejecutado por los países del Sur global. América del Sur ha sido la región más activa en cuanto a su formulación y ejecución, bien sea para obtener un mayor grado de autonomía política y económica en la definición de sus proyectos de desarrollo, o para mejorar su posicionamiento y visibilidad dentro del sistema internacional de cooperación al desarrollo. Tal es el caso de la implementación de las estrategias adoptadas por Brasil y Colombia en materia de cooperación, la cual será inicialmente definida como la manifestación de los intereses nacionales a través del diseño y puesta en marcha de su política exterior. Por lo anterior, el objetivo de este artículo es analizar la CSS, tanto de Brasil como de Colombia, como herramienta de política exterior a través de dos factores: la identidad y la expertise institucional.
Association(s) Between Objectively Measured Sedentary Behavior Patterns and Obesity Among Brazilian Adolescents
Authors: Werneck André O. , Silva Evelyn C.A. , Bueno Maria R.O. , Vignadelli Lidyane Z. , Oyeyemi Adewale L. , Romanzini Catiana L.P. , Ronque Enio R.V. , Romanzini Marcelo 
Published: November 2018

Purpose: To investigate the association between patterns of sedentary behavior and obesity indicators among adolescents. Methods: This was a cross-sectional study conducted among 389 adolescents (186 boys) aged 10–14 years. Body mass index, body fat (skinfolds), and waist circumference were adopted as outcomes. Sedentary behavior patterns (total time, bouts, and breaks) measured through accelerometry (GT3X and GT3X+; ActiGraph, Pensacola, FL) were adopted as exposures. Peak height velocity, moderate to vigorous physical activity (accelerometer), cardiorespiratory fitness (Léger test), sex, and chronological age were adopted as covariates. Linear regression models adjusted for covariates were used to determine associations between outcome and exposure variables. Results: The mean age of adolescents was 11.8 (0.7) years. Boys were more active than girls (P < .001). Accumulating shorter bouts (1–4 min) of sedentary behavior was negatively associated with body mass index (β = −0.050; 95% confidence interval [CI], −0.098 to −0.003) and waist circumference (β = −0.133; 95% CI, −0.237 to −0.028). Similarly, a higher number of breaks in sedentary behavior were negatively associated with body mass index (β = −0.160; 95% CI, −0.319 to −0.001) and waist circumference (β = −0.412; 95% CI, −0.761 to −0.064). Conclusion: Shorter bouts of sedentary behavior (1–4 min) and a higher number of breaks of sedentary behavior were associated with lower adiposity. Our findings also suggest that breaking up sedentary time to ensure bouts of sedentary behavior are short might contribute to the prevention of obesity in adolescents.
High-Intensity Demands of 6-a-Side Small-Sided Games and 11-a-Side Matches in Youth Soccer Players
Authors: Goto Heita , King James A. 
Published: November 2018

Purpose: The purposes of the present study were to examine high-intensity running distance during 6-a-side small-sided games (SSGs) and 11-a-side matches (11M) in youth soccer players using speed and metabolic power approaches and the magnitude of difference between the high-intensity running distance calculated with the 2 approaches. Method: A total of 11 outfield players (age = 16.3 [0.6] y) performed SSGs with 3 pitch sizes (small SSG [SSGS], medium SSG, and large SSG [SSGL]) and 11M. A Global Positioning System (15 Hz) was employed to calculate total distance covered, distance covered at a speed ≥4.3 m·s−1 (TS), and metabolic power of ≥20 W·kg−1 (TP). Results: The total distance covered increased from SSGS through to SSGL (P < .001) and was greater during 11M and SSGL compared with other SSGs (P < .01). TS and TP increased from SSGS (TS vs TP = 98 [55] vs 547 [181] m) through to SSGL (538 [167] vs 1050 [234] m; P < .001). TS and TP during 11M (370 [122] vs 869 [233] m) was greater than SSGS (P < .001 for both) and less than SSGL (P < .05 for both). The magnitude of difference between TS and TP (as a percentage) was lower with an increase in pitch size during SSGs and was greater in SSGS (615% [404%]; P < .001), medium SSG (195% [76%]; P < .05), and smaller in SSGL (102% [33%]; P < .01) compared with 11M (145% [53%]). Conclusion: SSGs can replicate the high-intensity demands of 11M and the speed approach underestimates the high-intensity demands of SSGs and 11M compared with the metabolic power approach.
Impaired proteostasis in senescent vascular endothelial cells: a perspective on estrogen and oxidative stress in the aging vasculature
Authors: Hwang HyunTae V. , Lin Yun , Rebuffatti Michelle N. , Tran Darlene T. , Lee Lily , Gomes Aldrin V. , Li Chin-Shang , Knowlton Anne A. 
Published: November 2018

The heat shock response is an important cytoprotective mechanism for protein homeostasis and is an essential protective response to cellular stress and injury. Studies on changes in the heat shock response with aging have been mixed with regard to whether it is inhibited, and this, at least in part, reflects different tissues and different models. Cellular senescence is a key feature in aging, but work on the heat shock response in cultured senescent (SEN) cells has largely been limited to fibroblasts. Given the prevalence of oxidative injury in the aging cardiovascular system, we investigated whether SEN primary human coronary artery endothelial cells have a diminished heat shock response and impaired proteostasis. In addition, we tested whether this downregulation of heat shock response can be mitigated by 17β-estradiol (E2), which has a critical cardioprotective role in women, as we have previously reported that E2improves the heat shock response in endothelial cells (Hamilton KL, Mbai FN, Gupta S, Knowlton AA. Arterioscler Thromb Vasc Biol 24: 1628–1633, 2004). We found that SEN endothelial cells, despite their unexpectedly increased proteasome activity, had a diminished heat shock response and had more protein aggregation than early passage cells. SEN cells had increased oxidative stress, which promoted protein aggregation. E2treatment did not decrease protein aggregation or improve the heat shock response in either early passage or SEN cells. In summary, cellular senescence in adult human endothelial cells is accompanied by increased oxidative stress and a blunting of proteostasis, and E2did not mitigate these changes.NEW & NOTEWORTHY Senescent human endothelial cells have a diminished heat shock response and increased protein aggregates. Senescent human endothelial cells have increased basal oxidative stress, which increases protein aggregates. Physiological level of 17β-estradiol did not improve proteostasis in endothelial cells.Listen to this article's corresponding podcast at https://ajpheart.podbean.com/e/proteostasis-in-senescent-endothelial-cells/ .
Role of renin-angiotensin system antagonists in the prevention of bevacizumab- and sunitinib-mediated cardiac dysfunction
Authors: Mozolevska Viktoriya , Schwartz Anna , Cheung David , Goyal Vineet , Shaikh Bilal , Dingman Bella , Kim Esther , Mittal Ishika , Asselin Chantal Y. , Edel Andrea , Ravandi Amir , Thliveris James , Singal Pawan K. , Czaykowski Piotr , Jassal Davinder S. 
Published: November 2018

Although anticancer systemic therapy agents clearly lead to improved survival in patients with cancer, these can come at the cost of serious complications including cardiotoxicity. Two types of targeted systemic therapies currently in use for colorectal cancer (CRC) and renal cell cancer (RCC), respectively, include the vascular endothelial growth factor inhibitor bevacizumab (BVZ) and the tyrosine kinase inhibitor sunitinib (SNT). Despite the beneficial effects of BVZ and SNT in improving clinical outcomes in the settings of CRC and RCC, there is an increased risk of cardiac dysfunction. The aim of the present study was to determine whether prophylactic administration of renin-angiotensin system (RAS) inhibitors would attenuate the cardiotoxic side effects of BVZ or SNT in a chronic in vivo murine model. A total of 194 wild-type C57Bl/6 male mice received: 1) 0.9% saline, 2) BVZ (10 mg·kg−1·wk−1), or 3) SNT (40 mg·kg−1·day−1) for 4 wk. Within each arm, mice received daily prophylactic treatment with hydralazine (0.05 mg/ml), aliskiren (50 mg/kg), perindopril (4 mg/kg), or valsartan (2 mg/kg). Although hydralazine effectively lowered blood pressure in BVZ- or SNT-treated mice, it did not prevent left ventricular systolic dysfunction. Prophylactic administration of aliskiren, perindopril, or valsartan prevented adverse cardiovascular remodeling in mice treated with either BVZ or SNT. The addition of RAS antagonists also downregulated expression of phosphorylated p38 and Bcl-2-like 19-kDa interacting protein 3 in SNT-treated mice. In our chronic in vivo murine model, RAS antagonists partially attenuated the development of BVZ- or SNT-mediated cardiac dysfunction. Future clinical studies are warranted to investigate the cardioprotective effects of prophylactic treatment with RAS inhibitors in the settings of CRC and RCC. NEW & NOTEWORTHY In the evolving field of cardio-oncology, bevacizumab and sunitinib improve clinical outcomes in the settings of metastatic colorectal cancer and renal cell cancer, respectively. These anticancer drugs, however, are associated with an increased risk of cardiotoxicity. The prophylactic administration of renin-angiotensin system antagonists is partially cardioprotective against bevacizumab- and sunitinib-mediated cardiac dysfunction.
Peri/epicellular protein disulfide isomerase-A1 acts as an upstream organizer of cytoskeletal mechanoadaptation in vascular smooth muscle cells
Authors: Tanaka Leonardo Y. , Araujo Thaís L. S. , Rodriguez Andres I. , Ferraz Mariana S. , Pelegati Vitor B. , Morais Mauro C. C. , Santos Aline M. dos , Cesar Carlos L. , Ramos Alexandre F. , Alencar Adriano M. , Laurindo Francisco R. M. 
Published: November 2018

Although redox processes closely interplay with mechanoresponses to control vascular remodeling, redox pathways coupling mechanostimulation to cellular cytoskeletal organization remain unclear. The peri/epicellular pool of protein disulfide isomerase-A1 (pecPDIA1) supports postinjury vessel remodeling. Using distinct models, we investigated whether pecPDIA1 could work as a redox-dependent organizer of cytoskeletal mechanoresponses. In vascular smooth muscle cells (VSMCs), pecPDIA1 immunoneutralization impaired stress fiber assembly in response to equibiaxial stretch and, under uniaxial stretch, significantly perturbed cell repositioning perpendicularly to stretch orientation. During cyclic stretch, pecPDIA1 supported thiol oxidation of the known mechanosensor β1-integrin and promoted polarized compartmentalization of sulfenylated proteins. Using traction force microscopy, we showed that pecPDIA1 organizes intracellular force distribution. The net contractile moment ratio of platelet-derived growth factor-exposed to basal VSMCs decreased from 0.90 ± 0.09 (IgG-exposed controls) to 0.70 ± 0.08 after pecPDI neutralization ( P < 0.05), together with an enhanced coefficient of variation for distribution of force modules, suggesting increased noise. Moreover, in a single cell model, pecPDIA1 neutralization impaired migration persistence without affecting total distance or velocity, whereas siRNA-mediated total PDIA1 silencing disabled all such variables of VSMC migration. Neither expression nor total activity of the master mechanotransmitter/regulator RhoA was affected by pecPDIA1 neutralization. However, cyclic stretch-induced focal distribution of membrane-bound RhoA was disrupted by pecPDI inhibition, which promoted a nonpolarized pattern of RhoA/caveolin-3 cluster colocalization. Accordingly, FRET biosensors showed that pecPDIA1 supports localized RhoA activity at cell protrusions versus perinuclear regions. Thus, pecPDI acts as a thiol redox-dependent organizer and noise reducer mechanism of cytoskeletal repositioning, oxidant generation, and localized RhoA activation during a variety of VSMC mechanoresponses. NEW & NOTEWORTHY Effects of a peri/epicellular pool of protein disulfide isomerase-A1 (pecPDIA1) during mechanoregulation in vascular smooth muscle cells (VSMCs) were highlighted using approaches such as equibiaxial and uniaxial stretch, random single cell migration, and traction force microscopy. pecPDIA1 regulates organization of the cytoskeleton and minimizes the noise of cell alignment, migration directionality, and persistence. pecPDIA1 mechanisms involve redox control of β1-integrin and localized RhoA activation. pecPDIA1 acts as a novel organizer of mechanoadaptation responses in VSMCs.
Atrial fibrillation and electrophysiology in transgenic mice with cardiac-restricted overexpression of FKBP12
Authors: Pan Zhenwei , Ai Tomohiko , Chang Po-Cheng , Liu Ying , Liu Jijia , Maruyama Mitsunori , Homsi Mohamed , Fishbein Michael C. , Rubart Michael , Lin Shien-Fong , Xiao Deyong , Chen Hanying , Chen Peng-Sheng , Shou Weinian , Li Bai-Yan 
Published: November 2018

Cardiomyocyte-restricted overexpression of FK506-binding protein 12 transgenic (αMyHC-FKBP12) mice develop spontaneous atrial fibrillation (AF). The aim of the present study is to explore the mechanisms underlying the occurrence of AF in αMyHC-FKBP12 mice. Spontaneous AF was documented by telemetry in vivo and Langendorff-perfused hearts of αMyHC-FKBP12 and littermate control mice in vitro. Atrial conduction velocity was evaluated by optical mapping. The patch-clamp technique was applied to determine the potentially altered electrophysiology in atrial myocytes. Channel protein expression levels were evaluated by Western blot analyses. Spontaneous AF was recorded in four of seven αMyHC-FKBP12 mice but in none of eight nontransgenic (NTG) controls. Atrial conduction velocity was significantly reduced in αMyHC-FKBP12 hearts compared with NTG hearts. Interestingly, the mean action potential duration at 50% but not 90% was significantly prolonged in αMyHC-FKBP12 atrial myocytes compared with their NTG counterparts. Consistent with decreased conduction velocity, average peak Na+ current ( INa) density was dramatically reduced and the INa inactivation curve was shifted by approximately +7 mV in αMyHC-FKBP12 atrial myocytes, whereas the activation and recovery curves were unaltered. The Nav1.5 expression level was significantly reduced in αMyHC-FKBP12 atria. Furthermore, we found increases in atrial Cav1.2 protein levels and peak L-type Ca2+ current density and increased levels of fibrosis in αMyHC-FKBP12 atria. In summary, cardiomyocyte-restricted overexpression of FKBP12 reduces the atrial Nav1.5 expression level and mean peak INa, which is associated with increased peak L-type Ca2+ current and interstitial fibrosis in atria. The combined electrophysiological and structural changes facilitated the development of local conduction block and altered action potential duration and spontaneous AF. NEW & NOTEWORTHY This study addresses a long-standing riddle regarding the role of FK506-binding protein 12 in cardiac physiology. The work provides further evidence that FK506-binding protein 12 is a critical component for regulating voltage-gated sodium current and in so doing has an important role in arrhythmogenic physiology, such as atrial fibrillation.
Age-related differences in the cutaneous vascular response to exogenous angiotensin II
Authors: Lang James A. , Krajek Alex C. 
Published: November 2018

Angiotensin II (ANG II) is locally produced in human skin and contributes to the reflex vasoconstriction (VC) response in aged but not young skin. We hypothesized that the exogenous ANG II-mediated VC response would be greater in older adults and would be affected by inhibition of adrenoreceptor or ANG II type II receptor (AT2R) pathways. Three microdialysis (MD) fibers were placed in the forearm skin of 11 young (26 ± 3 yr) and 11 older (68 ± 4 yr) individuals for perfusion of 1) Ringer solution (control), 2) adrenoreceptor blockade with yohimbine + propranolol, and 3) AT2R inhibition with PD-123319. ANG II was then added to the perfusates at eight graded dose concentrations ranging from 10−10 to 10−3 M. Laser Doppler flux was measured at each MD site, and cutaneous vascular conductance (CVC) was calculated as CVC =  laser Doppler flux/mean arterial pressure and normalized to baseline CVC values collected before ANG II perfusion (%ΔCVCbaseline). At the control site, older adults (−34 ± 4%ΔCVCbaseline) exhibited a greater peak VC compared with young adults (−22 ± 2%ΔCVCbaseline, P < 0.05), which was attenuated with adrenoreceptor blockade. Young skin exhibited a vasodilation in response to lower ANG II doses that was inhibited with AT2R inhibition. AT2R inhibition also increased the VC response to higher ANG II doses such that young skin responded similarly to older skin. These results indicate that ANG II has a greater VC influence in older than young individuals. Furthermore, ANG II may be affecting multiple targets, including adrenergic and AT2R pathways. NEW & NOTEWORTHY Intradermal perfusion of successive doses of angiotensin II (ANG II) revealed a role for ANG II type II receptors and dose-dependent, ANG II-mediated vasodilation in young but not older adults. In contrast, older adults exhibited greater vasoconstriction for a given dose of ANG II. The increased vasoconstriction in older adults was subsequently blunted with adrenoreceptor blockade, which indicates an interaction between ANG II and adrenergic signaling pathways in the cutaneous microcirculation.