cometadata/datacite-titles-descriptions-related-identifiers huggingface dataset:
DOI: 10.6084/m9.figshare.5241589
title: Erratum: Changes in Memory before and after Stroke Differ by Age and Sex, but Not by Race

description: <b><i>Background:</i></b> Post-stroke memory impairment is more common among older adults, women and blacks. It is unclear whether post-stroke differences reflect differential effects of stroke per se or differences in prestroke functioning. We compare memory trajectories before and after stroke by age, sex and race. <b><i>Methods:</i></b> Health and Retirement Study participants aged ≥50 years (n = 17,341), with no stroke history at baseline, were interviewed biennially up to 10 years for first self- or proxy-reported stroke (n = 1,574). Segmented linear regression models were used to compare annual rates of memory change before and after stroke among 1,169 stroke survivors, 405 stroke decedents and 15,767 stroke-free participants. Effect modification was evaluated with analyses stratified by baseline age (≤70 vs. &gt;70), sex and race (white vs. nonwhite), and using interaction terms between age/sex/race indicators and annual memory change. <b><i>Results:</i></b> Older (&gt;70 years) adults experienced a faster memory decline before stroke (-0.19 vs. -0.10 points/year for survivors, -0.24 vs. -0.13 points/year for decedents, p &lt; 0.001 for both interactions), and among stroke survivors, larger memory decrements (-0.64 vs. -0.26 points, p &lt; 0.001) at stroke and faster memory decline (-0.15 vs. -0.07 points/year, p = 0.003) after stroke onset, compared to younger adults. Female stroke survivors experienced a faster prestroke memory decline than male stroke survivors (-0.14 vs. -0.10 points/year, p &lt; 0.001). However, no sex differences were seen for other contrasts. Although whites had higher post-stroke memory scores than nonwhites, race was not associated with rate of memory decline during any period of time; i.e. race did not significantly modify the rate of decline before or after stroke or the immediate effect of stroke on memory. <b><i>Conclusions:</i></b> Older age predicted worse memory change before, at and after stroke onset. Sex and race differences in post-stroke memory outcomes might be attributable to prestroke disparities, which may be unrelated to cerebrovascular disease.
DOI: 10.6084/m9.figshare.5241592
title: Erratum: Heme Oxygenase-1 and Acute Kidney Injury following Cardiac Surgery

description: <b><i>Background:</i></b> Intraoperative hemolysis and inflammation are associated with acute kidney injury (AKI) following cardiac surgery. Plasma-free hemoglobin induces heme oxygenase-1 (HO-1) expression. HO-1 degrades heme but increases in experimental models of AKI. This study tested the hypothesis that plasma HO-1 concentrations are associated with intraoperative hemolysis and are increased in patients that develop AKI following cardiac surgery. <b><i>Methods:</i></b> We measured plasma HO-1, free hemoglobin, and inflammatory markers in 74 patients undergoing cardiopulmonary bypass (CPB). AKI was defined as an<b> </b>increase in serum creatinine concentration of 50% or 0.3 mg/dl within 72 h of surgery. <b><i>Results:</i></b> Twenty-eight percent of patients developed AKI. HO-1 concentrations increased from 4.2 ± 0.2 ng/ml at baseline to 6.6 ± 0.5 ng/ml on postoperative day (POD) 1 (p &lt; 0.001). POD1 HO-1 concentrations were 3.1 ng/ml higher (95% CI 1.1-5.1) in AKI patients, as was the change in HO-1 from baseline to POD1 (4.4 ± 1.3 ng/ml in AKI patients vs. 1.5 ± 0.3 ng/ml in no-AKI patients, p = 0.006). HO-1 concentrations remained elevated in AKI patients even after controlling for AKI risk factors and preoperative drug therapy. Peak-free hemoglobin concentrations correlated with peak HO-1 concentrations on POD1 in patients that developed AKI (p = 0.02). Duration of CPB and post-CPB IL-6 and IL-10 concentrations were also associated with increased HO-1 on POD1. <b><i>Conclusion:</i></b> Plasma HO-1 is increased in patients that develop AKI, and CPB duration, hemolysis, and inflammation are associated with increased HO-1 concentrations following cardiac surgery. Strategies that alter hemolysis and HO-1 expression during cardiac surgery may affect risk for AKI.
DOI: 10.6084/m9.figshare.5241598.v1
title: Erratum: Preoperative Scoring and Limits of Prognostication: Functional Outcome after Surgical Decompression in Metastatic Spinal Cord Compression

description: <b><i>Objective:</i></b> To determine whether preoperative parameters correlate with the postoperative functional outcome in para- and tetraplegic patients with lung, kidney, breast and prostate cancer and metastatic spinal cord compression (MSCC). <b><i>Methods:</i></b> Information on 43 patients undergoing decompressive surgery and rehabilitation for MSCC was reviewed, including primary tumor, age, pre- and postoperative ambulation status, mobility subcategory of the Spinal Cord Injury Measure (mSCIM) and the Tokuhashi score. Differences between groups were analyzed by the nonparametric χ<sup>2</sup> test, and correlation coefficients (Spearman's rho) were computed. <b><i>Results:</i></b> Preoperative ambulation (p &lt; 0.001), the American Spinal Injury Association Impairment Scale (p &lt; 0.001) and the type of operation (p = 0.02) influenced the postoperative functional outcome. Any positive change in the mSCIM was influenced by preoperative ambulation (p &lt; 0.001). Patients with breast carcinoma showed significantly more positive changes in the mSCIM compared with other tumors (p = 0.002). No correlation was found between the treatment categories of the Tokuhashi score and the preoperative ambulatory status (p = 0.13) or the change in ambulation status (p = 0.29). <b><i>Conclusion:</i></b> The postoperative functional outcome of MSCC patients shows a linear association between the categories of the Tokuhashi score and the change in ambulation status. We recommend surgical decompression even in a palliative situation (Tokuhashi score 0-8) with the aim of optimizing the short-term rehabilitation outcome. © 2014 S. Karger AG, Basel
DOI: 10.6084/m9.figshare.5241604.v1
title: Erratum: Estradiol Modulates the Expression Pattern of Myosin Heavy Chain Subtypes via an ERα-Mediated Pathway in Muscle-Derived Tissues and Satellite Cells

description: <b><i>Background: </i></b>Muscle-derived satellite cells (MDSCs) express MHC molecules intimately related to muscle function, which is supposed to be affected by local estrogen (E<sub>2</sub>) levels. However, cellular targets and molecular mechanisms involved are poorly understood. <b><i>Methods: </i></b>Genioglossus (GG) muscle tissues and MDSCs were derived from SHAM, ovariectomized or ovariectomized and 17 β-estradiol injected rats (n=10 ⁄ group). ERα, ERβ, MHC expression and underlying regulatory mechanisms were investigated by RT-PCR, western blot and immunohistochemistry, inter alia upon selective antagonist exposure and Si-RNA transfection. MDSC viability and cell cycle were examined by MTT and flow cytometry. <b><i>Results: </i></b>E<sub>2</sub> upregulated MHC-I and downregulated MHC-IIb expression in MDSCs. E<sub>2</sub> mediated effects on these molecules were inhibited by ERα-selective antagonist MPP and si-ERα, whereas they persisted upon exposure to ERβ-selective antagonist PHTPP. ERα was significantly higher expressed in muscle tissues compared to ERβ. ER positive stainings were fewer in the ovariectomized than in the SHAM group. Injection of E<sub>2</sub> only increased the positive staining of ERα, but not of ERβ. <b><i>Conclusion: </i></b>Results suggest that E<sub>2</sub> regulates MHC expression mainly through an ERα-mediated pathway with opposing effects on MHC-I and MHC-IIb. Thus, different hormonal processes that impact muscular pathophysiology presumably govern the functional properties of these molecules.
DOI: 10.6084/m9.figshare.5241586
title: Erratum: BK Virus Replication in Patients with Anti-Neutrophil Cytoplasmic Antibody-Associated Vasculitis

description: <b><i>Background:</i></b> BK virus (BKV) is an important cause of renal dysfunction in kidney transplant (KTX) recipients. Immunosuppression intensity is a major risk factor for BKV replication in these patients. The prevalence of BKV replication in immunosuppressed patients with granulomatosis with polyangiitis (GPA) and microscopic polyangiitis (MPA) without transplant is not known. <b><i>Methods:</i></b> Consecutive patients (n = 37) with a diagnosis of GPA (n = 25) or MPA (n = 12) without history of KTX were evaluated for plasma BKV replication by quantitative PCR (group A). Descriptive data were collected. BKV replication in this nontransplant immunosuppressed vasculitis cohort was compared with a historical cohort of vasculitis KTX recipients (group B). <b><i>Results:</i></b> Group A patients had mean disease duration of 75 months. Mean age was 57 years and 54% were female. Mean time from vasculitis onset to BKV testing was 36 months, and 19/37 patients were tested within 24 months of induction therapy. At the time of BKV testing, 73% were on prednisone (P) with azathioprine, mycophenolate mofetil (MMF), methotrexate or leflunomide. None of the nontransplanted vasculitis patients had detectable plasma BKV. Among 35 patients in group B, 16 were tested for BKV; 5/16 (31%) had detectable virus in plasma at a mean of 6 months after TX (p = 0.002). Most (94%) were on maintenance therapy with MMF, P and tacrolimus. <b><i>Conclusion:</i></b> Immunosuppressed patients with GPA/MPA without KTX had no evidence of plasma BKV. However, BKV was common in GPA/MPA patients after KTX, suggesting that replication may be related to differences in immunosuppression, alloimmune activation or differences in host defense mechanisms.
DOI: 10.6084/m9.figshare.5241589.v1
title: Erratum: Changes in Memory before and after Stroke Differ by Age and Sex, but Not by Race

description: <b><i>Background:</i></b> Post-stroke memory impairment is more common among older adults, women and blacks. It is unclear whether post-stroke differences reflect differential effects of stroke per se or differences in prestroke functioning. We compare memory trajectories before and after stroke by age, sex and race. <b><i>Methods:</i></b> Health and Retirement Study participants aged ≥50 years (n = 17,341), with no stroke history at baseline, were interviewed biennially up to 10 years for first self- or proxy-reported stroke (n = 1,574). Segmented linear regression models were used to compare annual rates of memory change before and after stroke among 1,169 stroke survivors, 405 stroke decedents and 15,767 stroke-free participants. Effect modification was evaluated with analyses stratified by baseline age (≤70 vs. &gt;70), sex and race (white vs. nonwhite), and using interaction terms between age/sex/race indicators and annual memory change. <b><i>Results:</i></b> Older (&gt;70 years) adults experienced a faster memory decline before stroke (-0.19 vs. -0.10 points/year for survivors, -0.24 vs. -0.13 points/year for decedents, p &lt; 0.001 for both interactions), and among stroke survivors, larger memory decrements (-0.64 vs. -0.26 points, p &lt; 0.001) at stroke and faster memory decline (-0.15 vs. -0.07 points/year, p = 0.003) after stroke onset, compared to younger adults. Female stroke survivors experienced a faster prestroke memory decline than male stroke survivors (-0.14 vs. -0.10 points/year, p &lt; 0.001). However, no sex differences were seen for other contrasts. Although whites had higher post-stroke memory scores than nonwhites, race was not associated with rate of memory decline during any period of time; i.e. race did not significantly modify the rate of decline before or after stroke or the immediate effect of stroke on memory. <b><i>Conclusions:</i></b> Older age predicted worse memory change before, at and after stroke onset. Sex and race differences in post-stroke memory outcomes might be attributable to prestroke disparities, which may be unrelated to cerebrovascular disease.
DOI: 10.6084/m9.figshare.5241595.v1
title: Erratum: Serial Changes of Serum Endostatin and Angiopoietin-1 Levels in Preterm Infants with Severe Bronchopulmonary Dysplasia and Subsequent Pulmonary Artery Hypertension

description: <b><i>Background:</i></b> In bronchopulmonary dysplasia (BPD), disrupted angiogenesis may result from an imbalance between pro- and anti-angiogenic factors triggered by inflammation, leading to the late development of pulmonary artery hypertension (PAH). <b><i>Objectives:</i></b> To investigate whether the levels of serum endostatin (as an anti-angiogenic factor) and angiopoietin-1 (AP-1; as a pro-angiogenic factor) in early life are associated with the development of PAH in preterm infants with severe BPD. <b><i>Methods:</i></b> In this prospective cohort study, the levels of serum endostatin and AP-1 were measured from 56 infants (gestational age &lt;30 weeks or birth weight &lt;1,250 g) including severe BPD with PAH (‘PAH'; 15 infants) or without PAH (‘non-PAH'; 22 infants) and no/mild BPD (19 infants) groups on days 1, 7, 14, and 28 of life. <b><i>Results:</i></b> The PAH group consistently underwent more aggressive respiratory management than the non-PAH group, over 1 month after birth. The endostatin level and the ratio of endostatin to AP-1 on day 7 of life were significantly higher in the PAH group than in the non-PAH group or no/mild BPD groups (median 146.6 vs. 102.4/108.0 ng/ml; 62.1 vs. 18.6/14.9). The ratio of endostatin to AP-1 on day 1 was also significantly higher in the PAH group than in the no/mild BPD group (median 31.8 vs. 11.3). <b><i>Conclusions:</i></b> An increased serum endostatin to AP-1 ratio may reflect impaired angiogenesis that may preclude the development of PAH.
DOI: 10.6084/m9.figshare.5241580
title: Erratum: Hyperphosphorylation of Tau Protein in Hippocampus of Central Insulin-Resistant Rats is Associated with Cognitive Impairment

description: <b><i>Background: </i></b>Alzheimer's disease (AD) is one of the most common neurodegenerative diseases. Peripheral insulin resistance increases the risk for memory impairment and the development of AD. <b><i>Objective: </i></b>This study aims to assess changes in cognitive functions and the level of hyperphosphorylated tau proteins in central insulin-resistant rats. <b><i>Methods: </i></b>An <i>in vivo</i> central insulin-resistant (CIR) animal model was generated through intracerebroventricular injection of streptozotocin (STZ) into insulin-resistant (IR) rats that were induced by feeding a high-glucose/-protein/-fat diet. The Morris water maze test was used to assess changes in cognitive functions, pathological changes in the cornu ammonis 1 (CA1) region of the hippocampus were detected by immunohistochemistry, and the phosphorylation levels of tau proteins at specific sites were determined by Western blot analysis. <b><i>Results: </i></b>The escape latency time in the Morris water maze test was significantly prolonged; the number of phosphorylated tau proteins in the CA1 region of the hippocampus was significantly increased; and the phosphorylation levels of tau proteins at Ser199, Thr205, Thr212, Thr217 and Ser396 were significantly elevated in the CIR group compared with the IR and control groups. <b><i>Conclusion: </i></b>This study provides direct evidence that CIR plays an important role in AD pathogenesis by facilitating tau hyperphosphorylation.
DOI: 10.6084/m9.figshare.5241583
title: Erratum: Regulation of Autophagy by High Glucose in Human Retinal Pigment Epithelium

description: <b><i>Background: </i></b>Autophagy is a self-degradative process that is important for balancing sources of energy at critical times in development and in response to nutrient stress. Retinal pigment epithelium (RPE) works as the outer blood retina barrier and is vulnerable to energy stress-induced injury. However, the effect of high glucose treatment on autophagy is still unclear in RPE. <b><i>Methods: </i></b>Transmission electron microscopy was used to detect the generation of autophagosome. Small interfering RNA (siRNA) and MTT was used to determine the effect of autophagy on cell viability. Western blots and immunohistochemistry were used to detect the expression pattern of autophagic markers, including LC3 and p62. <b><i>Results: </i></b>High glucose treatment results in a significant increase in the generation of autophagosome and altered expression of LC3 and p62. High glucose-induced autophagy is independent of mTOR signaling, but is mainly regulated via ROS-mediated ER stress signaling. <b><i>Conclusion: </i></b>In the scenario of high glucose-induced oxidative stress, autophagy may be required for the removal of damaged proteins, and provide a default mechanism to prevent high glucose-induced injury in RPE. © 2014 S. Karger AG, Basel
DOI: 10.6084/m9.figshare.5241586.v1
title: Erratum: BK Virus Replication in Patients with Anti-Neutrophil Cytoplasmic Antibody-Associated Vasculitis

description: <b><i>Background:</i></b> BK virus (BKV) is an important cause of renal dysfunction in kidney transplant (KTX) recipients. Immunosuppression intensity is a major risk factor for BKV replication in these patients. The prevalence of BKV replication in immunosuppressed patients with granulomatosis with polyangiitis (GPA) and microscopic polyangiitis (MPA) without transplant is not known. <b><i>Methods:</i></b> Consecutive patients (n = 37) with a diagnosis of GPA (n = 25) or MPA (n = 12) without history of KTX were evaluated for plasma BKV replication by quantitative PCR (group A). Descriptive data were collected. BKV replication in this nontransplant immunosuppressed vasculitis cohort was compared with a historical cohort of vasculitis KTX recipients (group B). <b><i>Results:</i></b> Group A patients had mean disease duration of 75 months. Mean age was 57 years and 54% were female. Mean time from vasculitis onset to BKV testing was 36 months, and 19/37 patients were tested within 24 months of induction therapy. At the time of BKV testing, 73% were on prednisone (P) with azathioprine, mycophenolate mofetil (MMF), methotrexate or leflunomide. None of the nontransplanted vasculitis patients had detectable plasma BKV. Among 35 patients in group B, 16 were tested for BKV; 5/16 (31%) had detectable virus in plasma at a mean of 6 months after TX (p = 0.002). Most (94%) were on maintenance therapy with MMF, P and tacrolimus. <b><i>Conclusion:</i></b> Immunosuppressed patients with GPA/MPA without KTX had no evidence of plasma BKV. However, BKV was common in GPA/MPA patients after KTX, suggesting that replication may be related to differences in immunosuppression, alloimmune activation or differences in host defense mechanisms.
DOI: 10.6084/m9.figshare.5241574
title: Erratum: Hemodynamic Stabilizing Effects of L-Carnitine in Chronic Hemodialysis Patients

description: <b><i>Background:</i></b> The effects of L-carnitine on the hemodynamic state of chronic hemodialysis patients have been debated. In order to clarify the effect of administered L-carnitine on cardiac function and hypotensive episodes during the hemodialysis procedure, a randomized double-blind placebo-controlled study was performed for 3 months. <b><i>Methods and Results:</i></b> Twenty stable outpatients undergoing hemodialysis treatment were divided into two groups: controls (placebo) and treated patients (L-carnitine 900 mg p.o. daily). After 3 months, cardiac function was reevaluated by echocardiography, and hypotensive episodes during hemodialysis were assessed. Free and acyl carnitine levels increased significantly from 22.3 ± 7.1 to 140.3 ± 57.5 μmol/l and from 15.8 ± 2.8 to 94.8 ± 50.4 μmol/l, respectively, in the treated group. The ejection fraction significantly increased from 61.8 ± 16.0 to 64.4 ± 13.8% (p &lt; 0.05) in the treated group. However, there was no difference in other echocardiographic parameters between the two groups. Hypotensive episodes significantly decreased from 4.0 ± 1.7 to 1.3 ± 0.9 times per month (p &lt; 0.05), although patients' body weight did not change significantly. <b><i>Conclusions:</i></b> Beneficial effects of L-carnitine on the hemodynamic state of chronic hemodialysis patients were observed. L-Carnitine supplementation might be considered especially for chronic hemodialysis patients with unstable hemodynamic conditions.
DOI: 10.6084/m9.figshare.5241577
title: Erratum: Hypothalamic and Pituitary Clusterin Modulates Neurohormonal Responses to Stress

description: Clusterin is a sulfated glycoprotein abundantly expressed in the pituitary gland and hypothalamus of mammals. However, its physiological role in neuroendocrine function is largely unknown. In the present study, we investigated the effects of intracerebroventricular (ICV) administration of clusterin on plasma pituitary hormone levels in normal rats. Single ICV injection of clusterin provoked neurohormonal changes seen under acute stress condition: increased plasma adrenocorticotropic hormone (ACTH), corticosterone, GH and prolactin levels and decreased LH and FSH levels. Consistently, hypothalamic and pituitary clusterin expression levels were upregulated following a restraint stress, suggesting an involvement of endogenous clusterin in stress-induced neurohormonal changes. In the pituitary intermediate lobe, clusterin was coexpressed with proopiomelanocortin (POMC), a precursor of ACTH. Treatment of clusterin in POMC expressing AtT-20 pituitary cells increased basal and corticotropin-releasing hormone (CRH)-stimulated POMC promoter activities and intracellular cAMP levels. Furthermore, clusterin treatment triggered ACTH secretion from AtT-20 cells in a CRH-dependent manner, indicating that increased clusterin under stressful conditions may augment CRH-stimulated ACTH production and release. In summary, hypothalamic and pituitary clusterin may function as a modulator of neurohormonal responses under stressful conditions.
DOI: 10.6084/m9.figshare.5241577.v1
title: Erratum: Hypothalamic and Pituitary Clusterin Modulates Neurohormonal Responses to Stress

description: Clusterin is a sulfated glycoprotein abundantly expressed in the pituitary gland and hypothalamus of mammals. However, its physiological role in neuroendocrine function is largely unknown. In the present study, we investigated the effects of intracerebroventricular (ICV) administration of clusterin on plasma pituitary hormone levels in normal rats. Single ICV injection of clusterin provoked neurohormonal changes seen under acute stress condition: increased plasma adrenocorticotropic hormone (ACTH), corticosterone, GH and prolactin levels and decreased LH and FSH levels. Consistently, hypothalamic and pituitary clusterin expression levels were upregulated following a restraint stress, suggesting an involvement of endogenous clusterin in stress-induced neurohormonal changes. In the pituitary intermediate lobe, clusterin was coexpressed with proopiomelanocortin (POMC), a precursor of ACTH. Treatment of clusterin in POMC expressing AtT-20 pituitary cells increased basal and corticotropin-releasing hormone (CRH)-stimulated POMC promoter activities and intracellular cAMP levels. Furthermore, clusterin treatment triggered ACTH secretion from AtT-20 cells in a CRH-dependent manner, indicating that increased clusterin under stressful conditions may augment CRH-stimulated ACTH production and release. In summary, hypothalamic and pituitary clusterin may function as a modulator of neurohormonal responses under stressful conditions.