cometadata/datacite-titles-descriptions-related-identifiers huggingface dataset:
DOI: 10.6084/m9.figshare.5241379
title: Erratum: Mechanisms of Pleurodesis

description: Pleurodesis aims to obliterate the pleural space by producing extensive adhesion of the visceral and parietal pleura, in order to control relapse of either pleural effusions (mostly malignant) or pneumothorax. A tight and complete apposition between the two pleural layers is a necessary condition to obtain a successful pleurodesis, but – besides this mechanical aspect – there are many biological mechanisms that appear to be common to most of the sclerosing agents currently used. Following intrapleural application of the sclerosing agent, diffuse inflammation, pleural coagulation-fibrinolysis imbalance (favoring the formation of fibrin adhesions), recruitment and subsequent proliferation of fibroblasts, and collagen production are findings in the pleural space. The pleural mesothelial lining is the primary target for the sclerosant and plays a pivotal role in the whole pleurodesis process, including the release of several mediators like interleukin-8, transforming growth factor-β and basic fibroblast growth factor. When the tumor burden is high, normal mesothelial cells are scarce, and consequently the response to the sclerosing agent is decreased, leading to failure of pleurodesis. Also, the type of tumor in the pleural cavity may also affect the outcome of pleurodesis (diffuse malignant mesothelioma and metastatic lung carcinomas have a poorer response). There is general agreement that talc obtains the best results, and there are also preliminary experimental studies suggesting that it can induce apoptosis in tumor cells and inhibit angiogenesis, thus contributing to a better control of the malignant pleural effusion. There is concern about complications (possibly associated with talc but other agents as well) related to systemic inflammation and possible activation of the coagulation cascade. In order to prevent extrapleural talc dissemination, large-particle talc is recommended. Although it could – to some degree – interfere with the mechanisms leading to pleurodesis and a carefully balanced clinical decision has therefore to be made, prophylactic treatment with subcutaneous heparin is recommended during hospitalization (immediately before and after the pleurodesis procedure).
DOI: 10.6084/m9.figshare.5241376
title: Erratum: The Antioxidant N-Acetylcysteine Prevents the Mitochondrial Fragmentation Induced by Soluble Amyloid-F Peptide Oligomers

description: <i>Background:</i> Soluble amyloid-F peptide oligomers (AFOs), which are centrally involved in the pathogenesis of Alzheimer’s disease, trigger Ca<sup>2+</sup> influx through N-methyl-<i>D</i>-aspartate receptors and stimulate reactive oxygen species generation in primary hippocampal neurons. We have previously reported that AFOs promote Ca<sup>2+</sup> release mediated by ryanodine receptors (RyR), which in turn triggers mitochondrial fragmentation. We have also reported that the antioxidant N-acetylcysteine (NAC) prevents AFOs-induced Ca<sup>2+</sup> signal generation. <i>Objectives:</i> To determine if RyR-mediated Ca<sup>2+</sup> release activated by the specific agonist 4-chloro-m-cresol (4-CMC) induces fragmentation of the mitochondrial network, and to ascertain if NAC prevents the mitochondrial fragmentation induced by AFOs and/or 4-CMC. <i>Methods:</i> Mature primary rat hippocampal neurons were incubated for 24 h with sublethal concentrations of AFOs (500 n<i>M</i>) or for 1–3 h with 4-CMC (0.5–1 m<i>M</i>), w10 m<i>M</i> NAC. Mitochondrial morphology was assessed by confocal microscopy of fixed neurons stained with anti-mHsp70. Intracellular Ca<sup>2+</sup> levels were determined by time series microscopy of neurons preloaded with Fluo-4 AM. <i>Results:</i> Preincubation of neurons for 30 min with NAC prevented the mitochondrial fragmentation induced by AFOs or 4-CMC. In addition, we confirmed that preincubation with NAC abolished the stimulation of RyR-mediated Ca<sup>2+</sup> release induced by AFOs or 4-CMC. <i>Conclusion:</i> The present results strongly suggest that the general antioxidant NAC prevents AFO-induced mitochondrial fragmentation by preventing RyR-mediated Ca<sup>2+</sup>-induced Ca<sup>2+</sup> release. Copyright i 2012 S. Karger AG, Basel
DOI: 10.6084/m9.figshare.5241382.v1
title: Erratum: Granulocyte Colony-Stimulating Factor Improves Cerebrovascular Reserve Capacity by Enhancing Collateral Growth in the Circle of Willis

description: <i>Background and Purpose:</i> Restoration of cerebrovascular reserve capacity (CVRC) depends on the recruitment and positive outward remodeling of preexistent collaterals (arteriogenesis). With this study, we provide functional evidence that granulocyte colony-stimulating factor (G-CSF) augments therapeutic arteriogenesis in two animal models of cerebral hypoperfusion. We identified an effective dosing regimen that improved CVRC and stimulated collateral growth, thereby improving the outcome after experimentally induced stroke. <i>Methods:</i> We used two established animal models of (a) cerebral hypoperfusion (mouse, common carotid artery ligation) and (b) cerebral arteriogenesis (rat, 3-vessel occlusion). Following therapeutic dose determination, both models received either G-CSF, 40 µg/kg every other day, or vehicle for 1 week. Collateral vessel diameters were measured following latex angiography. Cerebrovascular reserve capacities were assessed after acetazolamide stimulation. Mice with left common carotid artery occlusion (CCAO) were additionally subjected to middle cerebral artery occlusion, and stroke volumes were assessed after triphenyltetrazolium chloride staining. Given the vital role of monocytes in arteriogenesis, we assessed (a) the influence of G-CSF on monocyte migration in vitro and (b) monocyte counts in the adventitial tissues of the growing collaterals in vivo. <i>Results:</i> CVRC was impaired in both animal models 1 week after induction of hypoperfusion. While G-CSF, 40 µg/kg every other day, significantly augmented cerebral arteriogenesis in the rat model, 50 or 150 µg/kg every day did not show any noticeable therapeutic impact. G-CSF restored CVRC in mice (5 ± 2 to 12 ± 6%) and rats (3 ± 4 to 19 ± 12%). Vessel diameters changed accordingly: in rats, the diameters of posterior cerebral arteries (ipsilateral: 209 ± 7–271 ± 57 µm; contralateral: 208 ± 11–252 ± 28 µm) and in mice the diameter of anterior cerebral arteries (185 ± 15–222 ± 12 µm) significantly increased in the G-CSF groups compared to controls. Stroke volume in mice (10 ± 2%) was diminished following CCAO (7 ± 4%) and G-CSF treatment (4 ± 2%). G-CSF significantly increased monocyte migration in vitro and perivascular monocyte numbers in vivo. <i>Conclusion:</i> G-CSF augments cerebral collateral artery growth, increases CVRC and protects from experimentally induced ischemic stroke. When comparing three different dosing regimens, a relatively low dosage of G-CSF was most effective, indicating that the common side effects of this cytokine might be significantly reduced or possibly even avoided in this indication.
DOI: 10.6084/m9.figshare.5241373
title: Erratum: Simultaneous Occurrence of Biphenotypic T Cell/Myeloid Lesions Involving t(12;13)(p13;q14) in a Pediatric Patient

description: This paper chronicles a 2-year-old girl who presented with acute leukemia/lymphoma syndrome of the T cell immunophenotype. At this time, the cytogenetic analysis of her bone marrow cells showed a reciprocal translocation between the short arm of chromosome 12 and the long arm of chromosome 13, t(12;13)(p13;q14). The immunophenotyping of bone marrow blast cells by flow cytometry revealed a population of cells positive for CD56, CD117, CD45, partial CD33, partial HLA-DR, CD13, CD7, CD2 and CD5. Therefore, a diagnosis of acute leukemia with a mixed T cell/myeloid phenotype was made. The patient had a poor response to classic T cell acute lymphocytic leukemia/lymphoma therapy; thus, her treatment was changed to a myeloid leukemia protocol, which produced a good response. She underwent a successful cord blood transplantation from an unrelated HLA partially matched donor. The coexistence of these two phenotypes prompts questions about the existence of clonal instability, which might influence the choice of therapy. The rarity of the t(12;13)(p13;q14) and the coexistence of T cell/myeloid markers suggest a nonrandom association. To the best of our knowledge, this is the first reported case in which a cell clone bearing a t(12;13)(p13;q14) translocation in a mixed T cell/myeloid lesion was detected.
DOI: 10.6084/m9.figshare.5241376.v1
title: Erratum: The Antioxidant N-Acetylcysteine Prevents the Mitochondrial Fragmentation Induced by Soluble Amyloid-F Peptide Oligomers

description: <i>Background:</i> Soluble amyloid-F peptide oligomers (AFOs), which are centrally involved in the pathogenesis of Alzheimer’s disease, trigger Ca<sup>2+</sup> influx through N-methyl-<i>D</i>-aspartate receptors and stimulate reactive oxygen species generation in primary hippocampal neurons. We have previously reported that AFOs promote Ca<sup>2+</sup> release mediated by ryanodine receptors (RyR), which in turn triggers mitochondrial fragmentation. We have also reported that the antioxidant N-acetylcysteine (NAC) prevents AFOs-induced Ca<sup>2+</sup> signal generation. <i>Objectives:</i> To determine if RyR-mediated Ca<sup>2+</sup> release activated by the specific agonist 4-chloro-m-cresol (4-CMC) induces fragmentation of the mitochondrial network, and to ascertain if NAC prevents the mitochondrial fragmentation induced by AFOs and/or 4-CMC. <i>Methods:</i> Mature primary rat hippocampal neurons were incubated for 24 h with sublethal concentrations of AFOs (500 n<i>M</i>) or for 1–3 h with 4-CMC (0.5–1 m<i>M</i>), w10 m<i>M</i> NAC. Mitochondrial morphology was assessed by confocal microscopy of fixed neurons stained with anti-mHsp70. Intracellular Ca<sup>2+</sup> levels were determined by time series microscopy of neurons preloaded with Fluo-4 AM. <i>Results:</i> Preincubation of neurons for 30 min with NAC prevented the mitochondrial fragmentation induced by AFOs or 4-CMC. In addition, we confirmed that preincubation with NAC abolished the stimulation of RyR-mediated Ca<sup>2+</sup> release induced by AFOs or 4-CMC. <i>Conclusion:</i> The present results strongly suggest that the general antioxidant NAC prevents AFO-induced mitochondrial fragmentation by preventing RyR-mediated Ca<sup>2+</sup>-induced Ca<sup>2+</sup> release. Copyright i 2012 S. Karger AG, Basel
DOI: 10.6084/m9.figshare.5241361
title: Erratum: Comparable Analysis of Outcomes for Allogeneic Peripheral Blood Stem Cell Transplantation from Matched Related and Matched Unrelated Donors in Acute Myeloid Leukemia

description: This study compared the results of allogeneic peripheral blood stem cell transplantation (PBSCT) from unrelated and related donors in 142 consecutive patients with acute myeloid leukemia (AML). The cumulative incidence of acute graft-versus-host disease (GVHD) was 37.6% in the related PBSCT group and 53.7% in the unrelated PBSCT group. The cumulative incidence of extensive chronic GVHD was also higher in the unrelated PBSCT group (19.5%) than in the related PBSCT group (8.9%). The overall survival rate at 4 years was 62.4 ± 5.4 and 53.8 ± 1.2% (p = 0.535) in the related and unrelated PBSCT group, respectively. In a multivariate analysis, unrelated PBSCT was identified as a risk factor for the development of extensive chronic GVHD (hazard ratio = 3.019, p = 0.027). Unfavorable cytogenetics and the disease status at the time of transplantation were found to be related to overall survival. In the case of high-risk AML, the survival rate and relapse incidence were significantly better in the matched unrelated PBSCT group (p = 0.047 and 0.039, respectively). In conclusion, the allogeneic PBSCT outcomes for AML were comparable in the matched related and matched unrelated groups. Nonetheless, for high-risk AML patients, matched unrelated PBSCT was found to be preferable to matched related PBSCT.
DOI: 10.6084/m9.figshare.5241364
title: Erratum: Development of the Penile Urethra in the Tammar Wallaby

description: Hypospadias is increasingly common, and requires surgery to repair, but its aetiology is poorly understood. The marsupial tammar wallaby provides a unique opportunity to study hypospadias because penile differentiation occurs postnatally. Androgens are responsible for penile development in the tammar, but the majority of differentiation, in particular formation and closure of the urethral groove forming the penile urethra in males, occurs when there is no measurable sex difference in the concentrations of testosterone, dihydrotestosterone or androstanediol in either the gonads or the circulation. Phalluses were examined morphologically from the sexually indifferent period (when androgens are high) to well after the time that the phallus becomes sexually dimorphic. We show that penile development and critical changes in the positioning of the urethra occur in the male phallus begin during an early window of time when androgens are high. Remodelling of the urethra in the male occurs between days 20–60. The critical period of time for the establishment urethral closure occurs during the earliest phases of penile development. This study suggests that there is an early window of time before day 60 when androgen imprinting must occur for normal penile development and closure of the urethral groove.
DOI: 10.6084/m9.figshare.5241367
title: Erratum: Novel Peritoneal Dialysis Solutions – What Are the Clinical Implications?

description: Novel low-glucose degradation products (GDP) peritoneal dialysis (PD) fluids have an improved biocompatibility profile as compared to standard fluids. Clinical studies suggest that their use may be associated with favorable clinical outcomes; however, large prospective randomized studies addressing clinical endpoints such as patient and technique survival are presently lacking. Nevertheless, as their only disadvantage is their cost, they are already being used as the standard treatment by many adult PD centers. This policy is also in line with the latest recommendations from the European Pediatric Dialysis Working Group which advises that conventional, single-chamber PD solutions should be replaced by PD solutions with reduced GDP content. The use of icodextrin, the glucose polymer PD solution, is recommended for patients with high or high-average peritoneal transport and/or ultrafiltration problems who otherwise would resort to hypertonic (3.86% glucose) exchanges.
DOI: 10.6084/m9.figshare.5241370
title: Erratum: Vasculopathy Related to Manic/Hypomanic Symptom Burden and First-Generation Antipsychotics in a Sub-Sample from the Collaborative Depression Study

description: <b><i>Background:</i></b> Mood disorders substantially increase the risk of cardiovascular disease, though the mechanisms are unclear. We assessed for a dose-dependent relationship between course of illness or treatment with vasculopathy in a well-characterized cohort. <b><i>Methods:</i></b> Participants with mood disorders were recruited for the National Institute of Mental Health Collaborative Depression Study (CDS) and followed prospectively. A cross-sectional metabolic and vascular function evaluation was performed on a sub-sample near completion after a mean follow-up of 27 years. <b><i>Results:</i></b> A total of 35 participants from the University of Iowa (33) and Washington University (2) sites of the CDS consented to a metabolic and vascular function assessment at the Iowa site. In multivariate linear regression, controlling for age, gender, and smoking, manic/hypomanic, but not depressive, symptom burden was associated with lower flow-mediated dilation. Cumulative exposure to antipsychotics and mood stabilizers was associated with elevated augmentation pressure and mean aortic systolic blood pressure. This appeared specifically related to first-generation antipsychotic exposure and mediated by increases in brachial systolic pressure. Although second-generation antipsychotics were associated with dyslipidemia and insulin resistance, they were not associated with vasculopathy. <b><i>Conclusions:</i></b> These results provide evidence that chronicity of mood symptoms contribute to vasculopathy in a dose-dependent fashion. Patients with more manic/hypomanic symptoms had poorer endothelial function. First-generation antipsychotic exposure was associated with arterial stiffness, evidenced by higher augmentation pressure, perhaps secondary to elevated blood pressure. Vascular phenotyping methods may provide a promising means of elucidating the mechanisms linking mood disorders to vascular disease.
DOI: 10.6084/m9.figshare.5241373.v1
title: Erratum: Simultaneous Occurrence of Biphenotypic T Cell/Myeloid Lesions Involving t(12;13)(p13;q14) in a Pediatric Patient

description: This paper chronicles a 2-year-old girl who presented with acute leukemia/lymphoma syndrome of the T cell immunophenotype. At this time, the cytogenetic analysis of her bone marrow cells showed a reciprocal translocation between the short arm of chromosome 12 and the long arm of chromosome 13, t(12;13)(p13;q14). The immunophenotyping of bone marrow blast cells by flow cytometry revealed a population of cells positive for CD56, CD117, CD45, partial CD33, partial HLA-DR, CD13, CD7, CD2 and CD5. Therefore, a diagnosis of acute leukemia with a mixed T cell/myeloid phenotype was made. The patient had a poor response to classic T cell acute lymphocytic leukemia/lymphoma therapy; thus, her treatment was changed to a myeloid leukemia protocol, which produced a good response. She underwent a successful cord blood transplantation from an unrelated HLA partially matched donor. The coexistence of these two phenotypes prompts questions about the existence of clonal instability, which might influence the choice of therapy. The rarity of the t(12;13)(p13;q14) and the coexistence of T cell/myeloid markers suggest a nonrandom association. To the best of our knowledge, this is the first reported case in which a cell clone bearing a t(12;13)(p13;q14) translocation in a mixed T cell/myeloid lesion was detected.
DOI: 10.6084/m9.figshare.5241361.v1
title: Erratum: Comparable Analysis of Outcomes for Allogeneic Peripheral Blood Stem Cell Transplantation from Matched Related and Matched Unrelated Donors in Acute Myeloid Leukemia

description: This study compared the results of allogeneic peripheral blood stem cell transplantation (PBSCT) from unrelated and related donors in 142 consecutive patients with acute myeloid leukemia (AML). The cumulative incidence of acute graft-versus-host disease (GVHD) was 37.6% in the related PBSCT group and 53.7% in the unrelated PBSCT group. The cumulative incidence of extensive chronic GVHD was also higher in the unrelated PBSCT group (19.5%) than in the related PBSCT group (8.9%). The overall survival rate at 4 years was 62.4 ± 5.4 and 53.8 ± 1.2% (p = 0.535) in the related and unrelated PBSCT group, respectively. In a multivariate analysis, unrelated PBSCT was identified as a risk factor for the development of extensive chronic GVHD (hazard ratio = 3.019, p = 0.027). Unfavorable cytogenetics and the disease status at the time of transplantation were found to be related to overall survival. In the case of high-risk AML, the survival rate and relapse incidence were significantly better in the matched unrelated PBSCT group (p = 0.047 and 0.039, respectively). In conclusion, the allogeneic PBSCT outcomes for AML were comparable in the matched related and matched unrelated groups. Nonetheless, for high-risk AML patients, matched unrelated PBSCT was found to be preferable to matched related PBSCT.
DOI: 10.6084/m9.figshare.5241364.v1
title: Erratum: Development of the Penile Urethra in the Tammar Wallaby

description: Hypospadias is increasingly common, and requires surgery to repair, but its aetiology is poorly understood. The marsupial tammar wallaby provides a unique opportunity to study hypospadias because penile differentiation occurs postnatally. Androgens are responsible for penile development in the tammar, but the majority of differentiation, in particular formation and closure of the urethral groove forming the penile urethra in males, occurs when there is no measurable sex difference in the concentrations of testosterone, dihydrotestosterone or androstanediol in either the gonads or the circulation. Phalluses were examined morphologically from the sexually indifferent period (when androgens are high) to well after the time that the phallus becomes sexually dimorphic. We show that penile development and critical changes in the positioning of the urethra occur in the male phallus begin during an early window of time when androgens are high. Remodelling of the urethra in the male occurs between days 20–60. The critical period of time for the establishment urethral closure occurs during the earliest phases of penile development. This study suggests that there is an early window of time before day 60 when androgen imprinting must occur for normal penile development and closure of the urethral groove.
DOI: 10.6084/m9.figshare.5241370.v1
title: Erratum: Vasculopathy Related to Manic/Hypomanic Symptom Burden and First-Generation Antipsychotics in a Sub-Sample from the Collaborative Depression Study

description: <b><i>Background:</i></b> Mood disorders substantially increase the risk of cardiovascular disease, though the mechanisms are unclear. We assessed for a dose-dependent relationship between course of illness or treatment with vasculopathy in a well-characterized cohort. <b><i>Methods:</i></b> Participants with mood disorders were recruited for the National Institute of Mental Health Collaborative Depression Study (CDS) and followed prospectively. A cross-sectional metabolic and vascular function evaluation was performed on a sub-sample near completion after a mean follow-up of 27 years. <b><i>Results:</i></b> A total of 35 participants from the University of Iowa (33) and Washington University (2) sites of the CDS consented to a metabolic and vascular function assessment at the Iowa site. In multivariate linear regression, controlling for age, gender, and smoking, manic/hypomanic, but not depressive, symptom burden was associated with lower flow-mediated dilation. Cumulative exposure to antipsychotics and mood stabilizers was associated with elevated augmentation pressure and mean aortic systolic blood pressure. This appeared specifically related to first-generation antipsychotic exposure and mediated by increases in brachial systolic pressure. Although second-generation antipsychotics were associated with dyslipidemia and insulin resistance, they were not associated with vasculopathy. <b><i>Conclusions:</i></b> These results provide evidence that chronicity of mood symptoms contribute to vasculopathy in a dose-dependent fashion. Patients with more manic/hypomanic symptoms had poorer endothelial function. First-generation antipsychotic exposure was associated with arterial stiffness, evidenced by higher augmentation pressure, perhaps secondary to elevated blood pressure. Vascular phenotyping methods may provide a promising means of elucidating the mechanisms linking mood disorders to vascular disease.