Reporting Compliance of Stroke Trials: Cross-Sectional Analysis

Malhotra, Konark; Rayi, Appaji; Khunger, Monica; Thompson, Stephanie; Liebeskind, David S

doi:10.1016/j.jstrokecerebrovasdis.2017.03.010

Cited by 9 publications

(9 citation statements)

References 31 publications

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“…However, the authors likely included phase 1 trials during their selection that was conducted between October 1, 2007, and July 1, 2014, and that suggests their lower dissemination rates. In contrast, we had performed similar comprehensive analyses based on completed stroke 4 and epilepsy 5 trials that were registered on ClinicalTrials.gov and observed higher dissemination rates (80% and 75%, respectively) compared with the study subcategories in Sreekrishnan et al 1 In Reply We are excited to hear that our article 1 stimulated a conversation regarding the dissemination of clinical trials and we are happy to provide further clarification regarding our work. Malhotra et al have keen observations regarding the way in which the trials were selected and analyzed, which include (1) that the use of "closed studies" may include trials that never completed recruitment and (2) that the inclusion of phase 1 studies may bias toward unpublished work.…”

Section: Reporting and Dissemination Of Clinical Trials In Neurologymentioning

confidence: 82%

“…While this could facilitate oxygen unloading from blood to tissues, it is notable that this can also reduce the uptake of oxygen from pulmonary alveoli to pulmonary capillary blood. 4 The implication of this reduction in oxygen affinity with the right shift of the dissociation curve to clinical practice remains unknown. However, what is known from several clinical studies is that there is a strong association of adverse effects, including mortality with acidosis.…”

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confidence: 99%

“…We agree with the authors and support their goals to promote trial registration into prospective repositories with an aim for a universal data-sharing platform. 4 Konark Malhotra, MD Appaji Rayi, MD David S. Liebeskind, MD…”

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confidence: 99%

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What is the Association With Dissociation?—Reply

2018

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PCO 2 > 45 mm Hg) with a pH level of less than 7.35. They excluded patients with a metabolic acidosis or alkalosis from their analysis, but it is unclear how they defined these 2 acid-base states. Patients with compensated hypercapnia may represent a group of patients with competing acid-base disorders or a cohort of patients who experienced a less grievous initial physiological insult, whereas hypercapnic acidosis may actually reflect an increased severity of injury. As such, patients' pH levels and compensatory status likely represent dependent variables rather than causal agents.This study provides an opportunity to highlight the importance of pH and the oxyhemoglobin dissociation curve within the context of microcirculatory resuscitation and cellular oxygen unloading. 2 According to the oxyhemoglobin dissociation curve, alkalemia discourages oxygen unloading at the cellular level, whereas acidemia encourages it. 3 Although acidbase abnormalities in cerebrospinal fluid alter cerebral blood flow, 4 to our knowledge, no studies have assessed the neurological association of serum pH, and alkalemia in particular, with oxygen unloading. Striving to normalize serological numbers as a surrogate for physiologic normality is a common force in critical care, especially when retrospective data like these support the attainment of "euboxia." While awaiting clinical data from a randomized prospective clinical trial that assesses the association of arterial pH with neurological outcomes in patients who have sustained a cerebral injury, we will continue to manage patients with postcerebral injuries using physiological principles that are associated with the hemoglobin dissociation curve along with other supporting measures. 5

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Section: Reporting and Dissemination Of Clinical Trials In Neurologymentioning

confidence: 82%

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confidence: 99%

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2018

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“… 4 Although several clinical trials have been conducted, there is no established treatment to reduce the neurological deficits caused by ischemic stroke. 5 , 6 Many patients suffering from stroke often remain disabled after active therapies. 7 Therefore, well understanding the specific mechanism in ischemic stroke will contribute to identifying and developing new therapeutic targets.…”

Section: Introductionmentioning

confidence: 99%

MiR-101 Protects Against the Cerebral I/R Injury Through Regulating JAK2/STAT3 Signaling Pathway

Guo

Shen

Yong

2021

NDT

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Background: Ischemic stroke is a devastating disease with very limited therapeutics. Although miR-101 has been reported to play crucial roles in various human diseases, its role in ischemic stroke remains unclear. Methods: Ischemia-reperfusion (I/R) injury neuronal cells and rat model with I/R injury were constructed. Viability and apoptosis of I/R model cells with miR-101 overexpression or downregulation were evaluated. Potential targets of miR-101 were predicted using miRNA database microRNA.org and confirmed using luciferase reporter assays. Meanwhile, JAK2 and p-STAT3 protein levels were evaluated by Western blot. In addition, rescue experiments (silencing of JAK2) were applied to determine the role of miR-101 in cerebral I/R injury. Results: MiR-101 was significantly downregulated in OGD/R-induced neuronal cells and brain tissues with I/R injury. MiR-101 overexpression (miR-101 mimics) significantly promoted viability and inhibited apoptosis of OGD/R-induced neuronal cells in vitro and efficiently protected rats from ischemic brain injury in vivo. By contrast, miR-101 inhibitor exacerbated growth defect, apoptosis, and ischemic brain injury. Luciferase reporter assay indicated that JAK2 was a direct target of mIR-101, and JAK2 silencing effectively reversed the miR-101 inhibitor-induced neuronal cell apoptosis in vitro and reduced cerebral infarction volume in vivo. Conclusion:Our study demonstrated that miR-101 efficiently protected neuronal cells from apoptosis and ischemic brain injury through regulating the JAK2/STAT3 signaling pathway, suggesting that miR-101 might be a potential target for treatment of ischemic stroke.

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“…Because of the narrow treatment time window and the side effects of rt-PA, the current treatment effect of stroke is not ideal. At present, several clinical trials have been carried out to identify the effective treatment of stroke, yet no effective pharmacological therapies have been found to protect damaged brain tissue after stroke 1. In recent years, neuroprotective agents have attracted much attention, mainly through blocking one or more steps of neuronal ischaemic cascade to play a neuroprotective role.…”

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confidence: 99%

Non-coding RNA and neuroinflammation: implications for the therapy of stroke

et al. 2019

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Stroke is the major leading cause of death and serious, long-term disability with major economic consequences. At present, the lack of rapid diagnostic, prognostic biomarkers and effective treatment methods are two major challenges facing stroke. Circular RNAs (circRNAs) are potential clinical biomarkers in central nervous system diseases. However, the potential role of circRNAs in neuroinflammation and neuron functional recovery in acute ischaemic stroke (AIS) remains largely unknown. This review aimed to give an overview of the function of circRNAs in AIS and summarise the latest achievements in this field.

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Reporting Compliance of Stroke Trials: Cross-Sectional Analysis

Cited by 9 publications

References 31 publications

What is the Association With Dissociation?—Reply

What is the Association With Dissociation?—Reply

MiR-101 Protects Against the Cerebral I/R Injury Through Regulating JAK2/STAT3 Signaling Pathway

Non-coding RNA and neuroinflammation: implications for the therapy of stroke

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