Miracle-dz/UniFAR-FTUs huggingface dataset:
Diagnostic Accuracy of Central Venous Catheter Confirmation by Bedside Ultrasound Versus Chest Radiography in Critically Ill Patients: A Systematic Review and Meta-Analysis

Objective: We performed a systematic review and meta-analysis to examine the accuracy of bedside ultrasound for confirmation of central venous catheter position and exclusion of pneumothorax compared with chest radiography. Data Sources: PubMed, Embase, Cochrane Central Register of Controlled Trials, reference lists, conference proceedings and ClinicalTrials.gov. Study Selection: Articles and abstracts describing the diagnostic accuracy of bedside ultrasound compared with chest radiography for confirmation of central venous catheters in sufficient detail to reconstruct 2 × 2 contingency tables were reviewed. Primary outcomes included the accuracy of confirming catheter positioning and detecting a pneumothorax. Secondary outcomes included feasibility, interrater reliability, and efficiency to complete bedside ultrasound confirmation of central venous catheter position. Data Extraction: Investigators abstracted study details including research design and sonographic imaging technique to detect catheter malposition and procedure-related pneumothorax. Diagnostic accuracy measures included pooled sensitivity, specificity, positive likelihood ratio, and negative likelihood ratio. Data Synthesis: Fifteen studies with 1,553 central venous catheter placements were identified with a pooled sensitivity and specificity of catheter malposition by ultrasound of 0.82 (0.77–0.86) and 0.98 (0.97–0.99), respectively. The pooled positive and negative likelihood ratios of catheter malposition by ultrasound were 31.12 (14.72–65.78) and 0.25 (0.13–0.47). The sensitivity and specificity of ultrasound for pneumothorax detection was nearly 100% in the participating studies. Bedside ultrasound reduced mean central venous catheter confirmation time by 58.3 minutes. Risk of bias and clinical heterogeneity in the studies were high. Conclusions: Bedside ultrasound is faster than radiography at identifying pneumothorax after central venous catheter insertion. When a central venous catheter malposition exists, bedside ultrasound will identify four out of every five earlier than chest radiography.
Differential Associations of Socioeconomic Status With Global Brain Volumes and White Matter Lesions in African American and White Adults: the HANDLS SCAN Study

Objective The aim of the study was to examine interactive relations of race and socioeconomic status (SES) to magnetic resonance imaging (MRI)–assessed global brain outcomes with previously demonstrated prognostic significance for stroke, dementia, and mortality. Methods Participants were 147 African Americans (AAs) and whites (ages 33–71 years; 43% AA; 56% female; 26% below poverty) in the Healthy Aging in Neighborhoods of Diversity across the Life Span SCAN substudy. Cranial MRI was conducted using a 3.0 T unit. White matter (WM) lesion volumes and total brain, gray matter, and WM volumes were computed. An SES composite was derived from education and poverty status. Results Significant interactions of race and SES were observed for WM lesion volume (b = 1.38; &eegr;2 = 0.036; p = .028), total brain (b = 86.72; &eegr;2 = 0.042; p < .001), gray matter (b = 40.16; &eegr;2 = 0.032; p = .003), and WM (b = 46.56; &eegr;2 = 0.050; p < .001). AA participants with low SES exhibited significantly greater WM lesion volumes than white participants with low SES. White participants with higher SES had greater brain volumes than all other groups (albeit within normal range). Conclusions Low SES was associated with greater WM pathology—a marker for increased stroke risk—in AAs. Higher SES was associated with greater total brain volume—a putative global indicator of brain health and predictor of mortality—in whites. Findings may reflect environmental and interpersonal stressors encountered by AAs and those of lower SES and could relate to disproportionate rates of stroke, dementia, and mortality.
Regulation of IRE1α by the small molecule inhibitor 4μ8c in hepatoma cells

Abstract The unfolded protein response (UPR) is activated in response to impairments of the folding environment in the endoplasmic reticulum (ER). The most conserved arm of the UPR, inositol-requiring ER-to-nucleus signaling protein (IRE1α), has been linked to the regulation of a diverse array of cellular processes including ER-associated degradation, inflammatory signaling, cell proliferation and membrane biogenesis. Recent studies have utilized the selective, small molecule inhibitor, 4μ8c, to examine the role of IRE1α endoribonuclease (RNase) activity in various cell types including multiple myeloma, mouse embryonic fibroblasts and pancreatic beta cells [1-5]. In the present study we utilized this inhibitor to examine the role of IRE1α RNase activity in hepatoma cells (H4IIE), specifically concentrating on cell proliferation and the identification of potential off target effects under both unstressed and stressed conditions. Experiments were performed in H4IIE hepatoma cells in the absence (control conditions (LG)) or presence (LG + Thapsigargin (Thap)) of ER stress. The presence of 4μ8c decreased IRE1α RNase activity, based on reduced splicing of X-box binding protein-1 (XBP1s) and regulated IRE1α-dependent decay of mRNA in both treatments and at concentrations ranging from 10-90 μM. Cell proliferation was significantly reduced at higher concentrations (> 60 μM 4μ8c) in unstressed cells and displayed a dose-response relationship with 4μ8c in both treatments. The presence of 4μ8c did not promote cytoxicity in either of the treatment conditions but higher concentrations of the inhibitor (60 μM) were associated with apparent off-target or compensatory responses that were not observed at 10 μM. Overall, the small-molecule inhibitor, 4μ8c is an effective inhibitor of IRE1α RNase activity in H4IIE cells. Potential off-target effects associated with this inhibitor require the use of multiple inhibitor concentrations in all experiments.
Cardiovascular response to prescribed detraining among recreational athletes.

Exercise-induced cardiac remodeling (EICR) and the attendant myocardial adaptations characteristic of the athlete's heart may regress during periods of exercise reduction or abstinence. The time course and mechanisms underlying this reverse remodeling, specifically the impact of concomitant plasma volume (PV) contraction on cardiac chamber size, remain incompletely understood. We therefore studied recreational runners ( n = 21, age 34 ± 7 yr; 48% male) who completed an 18-wk training program (~7 h/wk) culminating in the 2016 Boston Marathon after which total exercise exposure was confined to <2 h/wk (no single session >1 h) for 8 wk. Cardiac structure and function, exercise capacity, and PV were assessed at peak fitness (10-14 days before) and at 4 wk and 8 wk postmarathon. Mixed linear modeling adjusting for age, sex, V̇o2peak, and marathon finish time was used to compare data across time points. Physiological detraining was evidenced by serial reductions in treadmill performance. Two distinct phases of myocardial remodeling and hematological adaptation were observed. After 4 wk of detraining, there were significant reductions in PV (Δ -6.0%, P < 0.01), left ventricular (LV) wall thickness (Δ -8.1%, <0.05), LV mass (Δ -10.3%, P < 0.001), and right atrial area (Δ -8.2%, P < 0.001). After 8 wk of detraining, there was a significant reduction in right ventricle chamber size (end-diastolic area Δ = -8.0%, P < 0.05) without further concomitant reductions in PV or LV wall thickness. Abrupt reductions in exercise training stimulus result in a structure-specific time course of reverse cardiac remodeling that occurs largely independently of PV contraction. NEW & NOTEWORTHY Significant reverse cardiac remodeling, previously documented among competitive athletes, extends to recreational runners and occurs with a distinct time course. Initial reductions in plasma volume and left ventricular (LV) mass, driven by reductions in wall thickness, are followed by contraction of the right ventricle. Consistent with data from competitive athletes, LV chamber volumes appear less responsive to detraining and may be a more permanent adaptation to sport.
A Descriptive, Longitudinal Study of Quality of Life and Perceived Health Needs in Patients With Head and Neck Cancer

Patients with head and neck cancer have numerous concerns and symptoms in the first year of posttreatment survivorship and are especially vulnerable at the end of treatment and 1 month posttreatment. This article shares the findings of a descriptive, longitudinal study of health-related quality of life (HRQOL) in patients with head and neck cancer from the beginning of treatment through 12 months posttreatment. The primary objective of this study was to describe the symptom experience and health needs of patients receiving radiation for head and neck cancer to support the establishment of an advanced practitioner (AP) clinic for head and neck cancer survivors. Significant findings in this study showed HRQOL at the end of treatment was significantly lower than baseline (p < .001). Low scores persisted through 1 month, with gradual recovery by 12 months. Fatigue and anxiety had the highest mean scores, yet anxiety improved with time, whereas fatigue did not. Positive human papillomavirus status was statistically associated with higher anxiety. Socioeconomic status negatively impacted HRQOL. Themes of perceived health needs were managing oral symptoms, returning to a normal life, and regaining energy. The AP in oncology can play a pivotal role in providing comprehensive assessment, symptom management, health education, and supportive counseling in this population throughout treatment and survivorship.
LPA1 receptor–mediated thromboxane A2 release is responsible for lysophosphatidic acid‐induced vascular smooth muscle contraction

Lysophosphatidic acid (LPA) has been recognized recently as an endothelium‐dependent vasodilator, but several lines of evidence indicate that it may also stimulate vascular smooth muscle cells (VSMCs), thereby contributing to vasoregulation and remodeling. In the present study, mRNA expression of all 6 LPA receptor genes was detected in murine aortic VSMCs, with the highest levels of LPA1, LPA2, LPA4, and LPA6. In endothelium‐denuded thoracic aorta (TA) and abdominal aorta (AA) segments, 1‐oleoyl‐LPA and the LPA1–3 agonist VPC31143 induced dose‐dependent vasoconstriction. VPC31143‐induced AA contraction was sensitive to pertussis toxin (PTX), the LPA1&3 antagonist Ki16425, and genetic deletion of LPA1 but not that of LPA2 or inhibition of LPA3, by diacylglycerol pyro‐phosphate. Surprisingly, vasoconstriction was also diminished in vessels lacking cyclooxygenase‐1 [COX1 knockout (KO)] or the thromboxane prostanoid (TP) receptor (TP KO). VPC31143 increased thromboxane A2 (TXA2) release from TA of wild‐type, TP‐KO, and LPA2‐KO mice but not from LPA1‐KO or COX1‐KO mice, and PTX blocked this effect. Our findings indicate that LPA causes vasoconstriction in VSMCs, mediated by LPA1‐, Gi‐, and COX1‐dependent autocrine/paracrine TXA2 release and consequent TP activation. We propose that this new‐found interaction between the LPA/LPA1 and TXA2/TP pathways plays significant roles in vasoregulation, hemostasis, thrombosis, and vascular remodeling. —Dancs, P. T. , Ruisanchez, E. , Balogh, A. , Panta, C. R. , Miklós, Z. , Nüsing, R. M. , Aoki, J., Chun, J., Offermanns, S. , Tigyi, G. , Benyó, Z. LPA1 receptor‐mediated thromboxane A2 release is responsible for lysophos‐phatidic acid‐induced vascular smooth muscle contraction. FASEB J. 31, 1547–1555 (2017) www.fasebj. org
DNA Repair Interacts with Autophagy To Regulate Inflammatory Responses to Pulmonary Hyperoxia

Oxygen is supplied as a supportive treatment for patients suffering from acute respiratory distress syndrome. Unfortunately, high oxygen concentration increases reactive oxygen species generation, which causes DNA damage and ultimately cell death in the lung. Although 8-oxoguanine-DNA glycosylase (OGG-1) is involved in repairing hyperoxia-mediated DNA damage, the underlying molecular mechanism remains elusive. In this study, we report that ogg-1–deficient mice exhibited a significant increase of proinflammatory cytokines (TNF-α, IL-6, and IFN-γ) in the lung after being exposed to 95% oxygen. In addition, we found that ogg-1 deficiency downregulated (macro)autophagy when exposed to hyperoxia both in vitro and in vivo, which was evident by decreased conversion of LC3-I to LC3-II, reduced LC3 punctate staining, and lower Atg7 expression compared with controls. Using a chromatin immunoprecipitation assay, we found that OGG-1 associated with the promoter of Atg7, suggesting a role for OGG1 in regulation of Atg7 activity. Knocking down OGG-1 decreased the luciferase reporter activity of Atg7. Further, inflammatory cytokine levels in murine lung epithelial cell line cells were downregulated following autophagy induction by starvation and rapamycin treatment, and upregulated when autophagy was blocked using 3-methyladenine and chloroquine. atg7 knockout mice and Atg7 small interfering RNA-treated cells exhibited elevated levels of phospho–NF-κB and intensified inflammatory cytokines, suggesting that Atg7 impacts inflammatory responses to hyperoxia. These findings demonstrate that OGG-1 negatively regulates inflammatory cytokine release by coordinating molecular interaction with the autophagic pathway in hyperoxia-induced lung injury.
Outage optimal relay selection and power allocation for amplify-and-forward relaying networks

In this paper, we consider the relay selection and power allocation problem in an amplify-and-forward relaying network, the objective is to minimize the outage probability given that only mean channel gain information is known. We firstly show that relay selection is important in achieving the global optimal solution in addition to the power allocation. Based on this argument, we then propose to decompose the problem into two parts: relay selection and power allocation. For the relay selection problem, a novel scheme is designed to incrementally select relays according to their ordering of mean channel gain. Then for the given set of relays, the optimal power allocation for the source and relays are obtained by exploiting the special structure of the problem. Simulation results show that the proposed scheme outperforms existing schemes without relay selection, which is also very efficient since the results obtained by this scheme are very close to the optimal results achieved by exhaustive search.
Arterial Hypertension, Atrial Fibrillation, and Hyperaldosteronism: The Triple Trouble

Atrial fibrillation (AF) involves 1% to 2% of the adult general population, a rate that increases to 15% in those 80 years and above.1 Because of the aging of the general population, this epidemic of AF is expected to increase over the next decades2–4 and to impose an increasing burden on the healthcare system because of the need for life-long care and pharmacological treatment. Identification of the mechanisms underlying AF represents an unmet need and a first step toward developing more effective preventive measures. Arterial hypertension (HT) is tightly associated with AF, as originally reported in the Framingham Heart Study5 and thereafter confirmed by several studies.6–13 HT is a major predictor of AF, and 50% to 90% of AF patients have HT. Accumulating evidences point to a role for the renin–angiotensin–aldosterone system (RAAS) in the pathophysiology of cardiac inflammation, fibrosis, and hypertrophy.14–17 Aldosterone not only exerts well-known pressor effects, but also promotes inflammation, myocardial necrosis, cardiac collagen deposition, fibrosis, and left ventricular hypertrophy (LVH). 18,19 Accordingly, there is renewed interest in aldosterone as one of the major culprits leading to chamber remodeling and ultimately creating the stage for AF in hypertensive patients.15,17,20–25 The evidence supporting a role for aldosterone in AF was, however, derived from observational studies performed in patients with heart diseases that are known to cause AF. This leaves open the question of whether aldosterone triggers AF per se or only in the presence of structural heart disease. In recent years, 3 reviews examined the relation between aldosterone and AF: one focused on the antiarrhythmic potential of mineralocorticoid receptor (MR) antagonists in AF patients;26 another on the role of the MR in arrhythmias;27 and the last …
Cerebral blood flow MRI in the nondemented elderly is not predictive of post-operative delirium but is correlated with cognitive performance

Three-dimensional Arterial Spin Labeling (ASL) MRI was performed before surgery in a cohort of 146 prospectively enrolled subjects ≥ 70 years old scheduled to undergo elective surgery. We investigated the prospective association between ASL-derived measures of cerebral blood flow (CBF) before surgery with postoperative delirium incidence and severity using whole-brain and globally normalized voxel-wise analysis. We also investigated the cross-sectional association of CBF with patients’ baseline performance on specific neuropsychological tests, and with a composite general cognitive performance measure (GCP). Out of 146 subjects, 32 (22%) developed delirium. We found no significant association between global and voxel-wise CBF with delirium incidence or severity. We found the most significant positive associations between CBF of the posterior cingulate and precuneus and the Hopkins Verbal Learning Test – Revised total score, Visual Search and Attention Test (VSAT) score and the GCP composite. VSAT score was also strongly associated with right parietal lobe CBF. ASL can be employed in a large, well-characterized older cohort to examine associations between CBF and age-related cognitive performance. Although ASL CBF measures in regions previously associated with preclinical Alzheimer’s Disease were correlated with cognition, they were not found to be indicators of baseline pathology that may increase risk for delirium.
Modeling Laterality of the Globus Pallidus Internus in Patients With Parkinson's Disease

Neurosurgical interventions such as deep brain stimulation surgery of the globus pallidus internus (GPi) play an important role in the treatment of medically refractory Parkinson's disease (PD), and require high targeting accuracy. Variability in the laterality of the GPi across patients with PD has not been well characterized. The aim of this report is to identify factors that may contribute to differences in position of the motor region of GPi.
Epidemiology of antibiotic-resistant wound infections from six countries in Africa

Introduction Little is known about the antimicrobial susceptibility of common bacteria responsible for wound infections from many countries in sub-Saharan Africa. Methods We performed a retrospective review of microbial isolates collected based on clinical suspicion of wound infection between 2004 and 2016 from Mercy Ships, a non-governmental organisation operating a single mobile surgical unit in Benin, Congo, Liberia, Madagascar, Sierra Leone and Togo. Antimicrobial resistant organisms of interest were defined as methicillin-resistant Staphylococcus aureus (MRSA) or Enterobacteriaceae resistant to third-generation cephalosporins. Generalised mixed-effects models accounting for repeated isolates in a patient, potential clustering by case mix for each field service, age, gender and country were used to test the hypothesis that rates of antimicrobial resistance differed between countries. Results 3145 isolates from repeated field services in six countries were reviewed. In univariate analyses, the highest proportion of MRSA was found in Benin (34.6%) and Congo (31.9%), while the lowest proportion was found in Togo (14.3%) and Madagascar (14.5%); country remained a significant predictor in multivariate analyses (P=0.002). In univariate analyses, the highest proportion of third-generation cephalosporin-resistant Enterobacteriaceae was found in Benin (35.8%) and lowest in Togo (14.3%) and Madagascar (16.3%). Country remained a significant predictor for antimicrobial-resistant isolates in multivariate analyses (P=0.009). Conclusion A significant proportion of isolates from wound cultures were resistant to first-line antimicrobials in each country. Though antimicrobial resistance isolates were not verified in a reference laboratory and these data may not be representative of all regions of the countries studied, differences in the proportion of antimicrobial-resistant isolates and resistance profiles between countries suggest site-specific surveillance should be a priority and local antimicrobial resistance profiles should be used to guide empiric antibiotic selection.
Xenin Augments Duodenal Anion Secretion via Activation of Afferent Neural Pathways

Xenin-25, a neurotensin (NT)-related anorexigenic gut hormone generated mostly in the duodenal mucosa, is believed to increase the rate of duodenal ion secretion, because xenin-induced diarrhea is not present after Roux-en-Y gastric bypass surgery. Because the local effects of xenin on duodenal ion secretion have remained uninvestigated, we thus examined the neural pathways underlying xenin-induced duodenal anion secretion. Intravenous infusion of xenin-8, a bioactive C-terminal fragment of xenin-25, dose dependently increased the rate of duodenal HCO3− secretion in perfused duodenal loops of anesthetized rats. Xenin was immunolocalized to a subset of enteroendocrine cells in the rat duodenum. The mRNA of the xenin/NT receptor 1 (NTS1) was predominantly expressed in the enteric plexus, nodose and dorsal root ganglia, and in the lamina propria rather than in the epithelium. The serosal application of xenin-8 or xenin-25 rapidly and transiently increased short-circuit current in Ussing-chambered mucosa-submucosa preparations in a concentration-dependent manner in the duodenum and jejunum, but less so in the ileum and colon. The selective antagonist for NTS1, substance P (SP) receptor (NK1), or 5-hydroxytryptamine (5-HT)3, but not NTS2, inhibited the responses to xenin. Xenin-evoked Cl- secretion was reduced by tetrodotoxin (TTX) or capsaicin-pretreatment, and abolished by the inhibitor of TTX-resistant sodium channel Nav1.8 in combination with TTX, suggesting that peripheral xenin augments duodenal HCO3− and Cl− secretion through NTS1 activation on intrinsic and extrinsic afferent nerves, followed by release of SP and 5-HT. Afferent nerve activation by postprandial, peripherally released xenin may account for its secretory effects in the duodenum.
Profiling of Kidney Injury Biomarkers in Patients Receiving Cisplatin: Time‐dependent Changes in the Absence of Clinical Nephrotoxicity

The success of cisplatin‐containing regimens to treat solid tumors is limited, in part, by nephrotoxicity. In rodents, several urinary proteins have emerged that are sensitive indicators of cisplatin‐induced kidney injury. We sought to characterize time‐dependent changes in the urinary concentrations of 12 proteins, including kidney injury molecule‐1 (KIM‐1), calbindin, beta 2‐microglobulin (β2M), and trefoil factor 3 (TFF3) after cisplatin therapy. Urine was collected at baseline, 3 days (range, 2–5 days), and 10 days (range, 9–11 days) from 57 patients with solid tumors receiving outpatient cisplatin therapy (≥25 mg/m2). Serum creatinine was largely unchanged after cisplatin infusion. However, compared with baseline values, several novel biomarkers were significantly increased in the urine, including β2M, which was threefold higher by day 3 (P < 0.0001). Urinary KIM‐1 and TFF3 were elevated twofold by day 10 (P = 0.002 and P = 0.002, respectively), whereas calbindin levels were increased eightfold (P < 0.0001). We report novel time‐dependent changes in the urinary excretion of noninvasive markers of subclinical kidney injury after cisplatin treatment.