Research on the cause of death for severe stroke patients

Yuan, Meizhen; Li, Feng; Fang, Qin; Wang, Wei; Peng, Jiangtao; Qin, Deyu; Wang, Xuefeng; Liu, Guangwei

doi:10.1111/jocn.13954

Cited by 21 publications

(11 citation statements)

References 38 publications

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“…This factor has been explored but no conclusive result was found (Mees et al., 2016). Diagnosis of hypertension being advantageous for stroke survivors was not clinically plausible as it was a risk factor for further complication and mortality (Yuan et al., 2018). After further review of the data set, it was found that larger proportion of the stroke patients without hypertension diagnosis were of unspecified stroke type and were of lower initial FIM score.…”

Section: Discussionmentioning

confidence: 99%

Factors predicting clinically significant functional gain and discharge to home in stroke in-patients after rehabilitation – A retrospective cohort study

Chan

et al. 2020

Hong Kong Journal of Occupational Therapy

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Objective This study explored factors which predict stroke survivors who could achieve “clinically significant functional gain” and return home when being discharged from a local hospital after in-patient stroke rehabilitation programme. Methods This study included 562 inpatients with stroke who were residing at community dwellings before onset of stroke, and transferred to a convalescent hospital for rehabilitation from four acute hospitals over one year. The main outcome variables of prediction were (a) achieving “clinically significant functional gain” as measured by (a1) achievement of “minimal clinically important difference” (MCID) of improvement in Functional Independence Measure Motor Measure (FIM-MM)”, (a2) one or more level(s) of improvement in function group according to the patients’ FIM-MM, and (b) discharge to home. Sixteen predictor variables were identified and studied firstly with univariate binary logistic regression and those significant variables were then put into multivariate binary logistic regression. Results Based on multivariate regression, the significant predictors for “clinically significant functional gain” were: younger age <75 years old, higher Glasgow Coma Scale score at admission, with haemorrhagic stroke, intermediate FIM-MM function group. Those significant predictors for “discharge to home” were: living with family/caregivers before stroke, higher FIM score at admission, and one or more level(s) of improvement in FIM-MM function group. Conclusions This study identified findings consistent with overseas studies in additional to some new interesting findings. Early prediction of stroke discharge outcomes helps rehabilitation professionals and occupational therapists to focus on the use of appropriate intervention strategies and pre-discharge preparation.

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Section: Discussionmentioning

confidence: 99%

Factors predicting clinically significant functional gain and discharge to home in stroke in-patients after rehabilitation – A retrospective cohort study

Chan

et al. 2020

Hong Kong Journal of Occupational Therapy

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“…Our data indicates CD200-CD200R1-mediated regulation of immunity is essential for survival and improved behavioral outcome following stroke. Acute mortality rates from stroke are high, as the majority of severe stroke patients die within the first week of hospitalization [49]. Mirroring the clinical scenario, nearly half of the mice lacking CD200R1 did not survive the first week following a moderate ischemic brain injury, despite no difference in infarct size between the groups.…”

Section: Discussionmentioning

confidence: 99%

CD200-CD200R1 inhibitory signaling prevents spontaneous bacterial infection and promotes resolution of neuroinflammation and recovery after stroke

Ritzel

Mamun

Crapser

et al. 2019

J Neuroinflammation

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Background Ischemic stroke results in a robust inflammatory response within the central nervous system. As the immune-inhibitory CD200-CD200 receptor 1 (CD200R1) signaling axis is a known regulator of immune homeostasis, we hypothesized that it may play a role in post-stroke immune suppression after stroke. Methods In this study, we investigated the role of CD200R1-mediated signaling in stroke using CD200 receptor 1-deficient mice. Mice were subjected to a 60-min middle cerebral artery occlusion and evaluated at days 3 and 7, representing the respective peak and early resolution stages of neuroinflammation in this model of ischemic stroke. Infarct size and behavioral deficits were assessed at both time points. Central and peripheral cellular immune responses were measured using flow cytometry. Bacterial colonization was determined in lung tissue homogenates both after acute stroke and in an LPS model of systemic inflammation. Results In wild-type (WT) animals, CD200R1 was expressed on infiltrating monocytes and lymphocytes after stroke but was absent on microglia. Early after ischemia (72 h), CD200R1-knockout (KO) mice had significantly poorer survival rates and an enhanced susceptibility to spontaneous bacterial colonization of the respiratory tract compared to wild-type (WT) controls, despite no difference in infarct or neurological deficits. While the CNS inflammation was resolved by day 7 post-stroke in WT mice, brain-resident microglia and monocyte activation persisted in CD200R1-KO mice, accompanied by a delayed, augmented lymphocyte response. At this time point, CD200R1-KO mice displayed greater weight loss, more severe neurological deficits, and impaired motor function compared to WT. Systemically, CD200R1-KO mice exhibited signs of persistent infection including lymphopenia, T cell activation and memory conversion, and narrowing of the TCR repertoire. These findings were confirmed in a second model of acute neuroinflammation induced by systemic endotoxin challenge. Conclusion This study defines an essential role of CD200-CD200R1 signaling in stroke. Loss of CD200R1 led to high mortality, increased rates of post-stroke infection, and enhanced entry of peripheral leukocytes into the brain after ischemia, with no increase in infarct size. This suggests that the loss of CD200 receptor leads to enhanced peripheral inflammation that is triggered by brain injury. Electronic supplementary material The online version of this article (10.1186/s12974-019-1426-3) contains supplementary material, which is available to authorized users.

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“…Due to its rising overall incidence in recent years, ACI has become an important area of research. Clinical data indicate that patients with brain damage are often diagnosed with dysfunction and even failure of other organs [ 15 – 20 ]. The lung is one of the most vulnerable such organs [ 16 , 18 , 21 ].…”

Section: Introductionmentioning

confidence: 99%

Brain-Derived Glia Maturation Factor β Participates in Lung Injury Induced by Acute Cerebral Ischemia by Increasing ROS in Endothelial Cells

Zhang

Wang

et al. 2018

Neurosci. Bull.

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Brain damage can cause lung injury. To explore the mechanism underlying the lung injury induced by acute cerebral ischemia (ACI), we established a middle cerebral artery occlusion (MCAO) model in male Sprague-Dawley rats. We focused on glia maturation factor β (GMFB) based on quantitative analysis of the global rat serum proteome. Polymerase chain reaction, western blotting, and immunofluorescence revealed that GMFB was over-expressed in astrocytes in the brains of rats subjected to MCAO. We cultured rat primary astrocytes and confirmed that GMFB was also up-regulated in primary astrocytes after oxygen-glucose deprivation (OGD). We subjected the primary astrocytes to Gmfb RNA interference before OGD and collected the conditioned medium (CM) after OGD. We then used the CM to culture pulmonary microvascular endothelial cells (PMVECs) acquired in advance and assessed their status. The viability of the PMVECs improved significantly when Gmfb was blocked. Moreover, ELISA assays revealed an elevation in GMFB concentration in the medium after OGD. Cell cultures containing recombinant GMFB showed increased levels of reactive oxygen species and a deterioration in the state of the cells. In conclusion, GMFB is up-regulated in astrocytes after ACI, and brain-derived GMFB damages PMVECs by increasing reactive oxygen species. GMFB might thus be an initiator of the lung injury induced by ACI.Electronic supplementary materialThe online version of this article (10.1007/s12264-018-0283-x) contains supplementary material, which is available to authorized users.

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Research on the cause of death for severe stroke patients

Abstract: Aims and objectives: To explore the characteristics of mortality among severe stroke patients, analyse their causes of death and provide evidence for improving the survival rate of stroke patients.Background: Stroke is an important fatal and disabling disease that poses a large

Cited by 21 publications

References 38 publications

Factors predicting clinically significant functional gain and discharge to home in stroke in-patients after rehabilitation – A retrospective cohort study

Factors predicting clinically significant functional gain and discharge to home in stroke in-patients after rehabilitation – A retrospective cohort study

CD200-CD200R1 inhibitory signaling prevents spontaneous bacterial infection and promotes resolution of neuroinflammation and recovery after stroke

Brain-Derived Glia Maturation Factor β Participates in Lung Injury Induced by Acute Cerebral Ischemia by Increasing ROS in Endothelial Cells

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