scholarly journals Global hypoxic ischaemic injury

2021 ◽  
Author(s):  
Jeremy Jones ◽  
Andrew Kirby
Keyword(s):  
Ischaemic Injury

Toll-like Receptor-4: A New Target for Preterm Labour Pharmacotherapies?

2018 ◽  
Vol 24 (9) ◽  
pp. 960-973 ◽  
Author(s):  
Sarah A. Robertson ◽  
Hanan H. Wahid ◽  
Peck Yin Chin ◽  
Mark R. Hutchinson ◽  
Lachlan M. Moldenhauer ◽  
...  
Keyword(s):  
Preterm Birth ◽  
Preterm Delivery ◽  
Platelet Activating Factor ◽  
Neonatal Morbidity ◽  
Ischaemic Injury ◽  
E Coli ◽  
Normal Term ◽  
Inflammatory Activation ◽  
Cervical Disease ◽  
Term Labour

Inflammatory activation, a major driver of preterm birth and subsequent neonatal morbidity, is an attractive pharmacological target for new preterm birth therapeutics. Inflammation elicited by intraamniotic infection is causally associated with preterm birth, particularly in infants delivered ≤34 weeks’ gestation. However, sterile triggers of PTB, including placental ischaemic injury, uterine distention, cervical disease, or imbalance in the immune response, also act through inflammatory mediators released in response to tissue damage. Toll-like Receptors (TLRs) are critical upstream gate-keepers controlling the inflammatory activation that precedes preterm delivery, as well as in normal term labour. In particular, TLR4 is implicated for its capacity to sense and integrate a range of disparate infectious and sterile pro-inflammatory triggers, and so acts as a point-ofconvergence through which a range of infectious and sterile agents can activate and accelerate the parturition cascade. Recent studies point to the TLR4 signalling complex as a tractable target for the inhibition of fetal, placental & intraamniotic inflammatory cytokine production. Moreover, studies on mice show that novel small molecule antagonists of TLR4 signalling are highly effective in preventing preterm birth induced by bacterial mimetic LPS, heat-killed E. coli or the TLR4-dependent pro-inflammatory lipid, Platelet Activating Factor (PAF). In this review, we discuss the role of TLR4 in regulating the timing of birth and the potential utility of TLR4 antagonists as novel therapeutics for preterm delivery.

Analysis of the Clinical Diagnostic Value of GMFB in Cerebral Infarction

2020 ◽  
Vol 21 (10) ◽  
pp. 955-963
Author(s):  
Zhaohu Yuan ◽  
Zhiwu Yu ◽  
Yiyu Zhang ◽  
Huikuan Yang
Keyword(s):  
Myocardial Infarct ◽  
Diagnostic Value ◽  
Artery Occlusion ◽  
Response Dynamics ◽  
Stroke Patients ◽  
Ischaemic Injury ◽  
Neuronal Nuclei ◽  
Diagnosis And Prognosis ◽  
Maturation Factor ◽  
Injury And Repair

Background: Glial Maturation Factor Beta (GMFB) is a highly conserved brain-enriched protein implicated in immunoregulation, neuroplasticity and apoptosis, processes central to neural injury and repair following cerebral ischaemia. Therefore, we examined if changes in neurocellular GMFB expression and release can be used to assess brain injury following ischaemia. Methods and Results: Immunofluorescence staining, Western blotting, immunohistochemistry and ELISA were used to measure GMFB in cultured neurons and astrocytes, rat brain tissues and plasma samples from stroke model rats and stroke patients, while cell viability assays, TTC staining and micro- PET were used to assess neural cell death and infarct severity. Immunofluorescence and immunohistochemistry revealed GMFB expression mainly in astrocyte and neuronal nuclei but also in neuronal axons and dendrites. Free GMFB concentration increased progressively in the culture medium during hypoxia-hypoglycaemia treatment. Plasma GMFB concentration increased in rats subjected to middle cerebral artery occlusion (MCAO, a model of stroke-reperfusion) and in stroke patients. Plasma GMFB in MCAO model rats was strongly correlated with infarct size (R2=0.9582). Plasma GMFB concentration was also markedly elevated in stroke patients within 24 h of onset and remained elevated for more than one week. Conversely, plasma GMFB elevations were not significant in myocardial infarct patients and stroke patients without infarction. Conclusion: GMFB has the prerequisite stability, expression specificity and response dynamics to serve as a reliable indicator of ischaemic injury in animal models and stroke patients. Plasma GMFB may be a convenient non-invasive adjunct to neuroimaging for stroke diagnosis and prognosis.

scholarly journals Efficacy and safety of butylphthalide for patients who had acute ischaemic stroke receiving intravenous thrombolysis or endovascular treatment (BAST trial): study protocol for a randomised placebo-controlled trial

BMJ Open ◽  
2021 ◽  
Vol 11 (5) ◽  
pp. e045559
Author(s):  
Xuelei Zhang ◽  
Anxin Wang ◽  
Jing Yu Zhang ◽  
Baixue Jia ◽  
Xiaochuan Huo ◽  
...  
Keyword(s):  
Ischaemic Stroke ◽  
Endovascular Treatment ◽  
Functional Outcome ◽  
Acute Ischaemic Stroke ◽  
Controlled Trial ◽  
Intravenous Thrombolysis ◽  
Serious Adverse Events ◽  
Double Blind ◽  
Ischaemic Injury ◽  
Study Results

IntroductionAs a neuroprotective medication, butylphthalide (NBP) may help protect against cerebral ischaemic injury. However, evidence on whether NBP influences the outcomes of patients who had acute ischaemic stroke who are receiving revascularisation treatment is limited. This study aims to evaluate whether additional NBP therapy can improve the functional outcome of patients who receive intravenous recombinant tissue plasminogen activator and/or endovascular treatment (EVT).Methods and analysisThe study will be a randomised, double-blind, placebo-controlled, multiple-centre, parallel group trial. The sample size is estimated at 1200 patients. Eligible patients will be randomised at a 1:1 ratio to receive either NBP or placebo daily for 90 days, which will include 14 days of injections and 76 days of capsules. The first use of NBP/placebo will be started within 6 hours of onset of ischaemic stroke. The primary outcome is the functional outcome as assessed by the 90-day modified Rankin Scale, adjusted for baseline scores on the National Institutes of Health Stroke Scale. The primary safety outcome is the percentage of serious adverse events during the 90 days of treatment. This trial will determine whether NBP medication benefits patients who had acute ischaemic stroke who receive intravenous thrombolysis or EVT.Ethics and disseminationThe protocol was written according to the general ethical guidelines of the Declaration of Helsinki and approved by the Institutional Review Board/Ethics Committee of Beijing Tiantan Hospital, Capital Medical University with approval number KY 2018-003-02. Ethics committees of all participating sites have approved the study . Results of the study will be published in peer-reviewed scientific journals and shared in scientific presentations.Trial registration numberNCT03539445.

scholarly journals Publisher Correction: Exosome-eluting stents for vascular healing after ischaemic injury

2021 ◽  
Author(s):  
Shiqi Hu ◽  
Zhenhua Li ◽  
Deliang Shen ◽  
Dashuai Zhu ◽  
Ke Huang ◽  
...  
Keyword(s):  
Ischaemic Injury

scholarly journals Perivascular spaces and brain waste clearance systems: relevance for neurodegenerative and cerebrovascular pathology

2021 ◽  
Author(s):  
Kaylene Gouveia-Freitas ◽  
António J. Bastos-Leite
Keyword(s):  
Basal Ganglia ◽  
Lymphatic Vessels ◽  
Vascular Wall ◽  
Lymphatic Drainage ◽  
Basement Membranes ◽  
Amyloid Angiopathy ◽  
Perivascular Spaces ◽  
Functional Abnormality ◽  
Ischaemic Injury ◽  
Cerebrovascular Pathology

AbstractPerivascular spaces (PVS) of the brain, often called Virchow-Robin spaces, comprise fluid, cells and connective tissue, and are externally limited by astrocytic endfeet. PVS are involved in clearing brain waste and belong to the “glymphatic” system and/or the “intramural periarterial drainage” pathway through the basement membranes of the arteries. Related brain waste clearance systems include the blood–brain barrier, scavenger cells, cerebrospinal fluid, perineural lymphatic drainage pathways and the newly characterised meningeal lymphatic vessels. Any functional abnormality of PVS or related clearance systems might lead to accumulation of brain waste. It has been postulated that PVS enlargement can be secondary to accumulation of β-amyloid. Lack of integrity of the vascular wall, microbleeds, cerebral amyloid angiopathy (CAA) and enlarged PVS often occur in the preclinical stages of Alzheimer’s disease, preceding substantial brain atrophy. PVS enlargement in the form of état criblé at the basal ganglia has also been considered to reflect focal atrophy, most probably secondary to ischaemic injury, based upon both pathological and imaging arguments. In addition, distinct topographic patterns of enlarged PVS are related to different types of microangiopathy: CAA is linked to enlarged juxtacortical PVS, whereas subjects with vascular risk factors tend to have enlarged PVS in the basal ganglia. Therefore, enlarged PVS are progressively being regarded as a marker of neurodegenerative and cerebrovascular pathology. The present review addresses the evolving concept of PVS and brain waste clearance systems, the potential relevance of their dysfunction to neurodegenerative and cerebrovascular pathology, and potential therapeutic approaches of interest.

Paradoxical resistance to ischaemic injury in hearts of NHE1-transgenic mice

2007 ◽  
Vol 42 (6) ◽  
pp. S196
Author(s):  
Alexandra Cook ◽  
Stefan Engelhardt ◽  
Metin Avkiran
Keyword(s):  
Transgenic Mice ◽  
Ischaemic Injury

Mechanisms of renal ischaemic injury and their clinical impact

2005 ◽  
Vol 95 (7) ◽  
pp. 948-950 ◽  
Author(s):  
Ithaar H. Derweesh ◽  
Andrew C. Novick
Keyword(s):  
Clinical Impact ◽  
Ischaemic Injury

Recovery from Acute Ischaemic Renal Failure is Accelerated by Des-(1–3)-Insulin-Like Growth Factor-1

1994 ◽  
Vol 86 (6) ◽  
pp. 709-714 ◽  
Author(s):  
Ross Clark ◽  
Deborah Mortensen ◽  
Ralph Rabkin
Keyword(s):  
Renal Failure ◽  
Acute Renal Failure ◽  
Growth Factor ◽  
Fractional Excretion ◽  
Insulin Like Growth Factor ◽  
Ischaemic Injury ◽  
Beneficial Effects ◽  
Nitrogen Levels ◽  
Renal Tubular Cells ◽  
Renal Tubular

1. Acute renal failure carries a high risk of morbidity and mortality, so there is a need for agents that minimize renal injury after an insult and that hasten repair. Insulin-like growth factor-1 is mitogenic for renal tubular cells; in normal kidneys it has haemodynamic effects and it is potently anabolic. We tested the theory that insulin-like growth factor-1 may be of use in the treatment of acute renal failure by administering recombinant des-(1–3)-insulin-like growth factor-1, a truncated form of insulin-like growth factor-1, which occurs naturally. Ischaemic renal failure was induced in normal rats by occluding both renal pedicles for 60 min. Then des-(1–3)-insulin-like growth factor-1 (0.8 mg day−1 kg−1) or vehicle was given by subcutaneous minipump for 7 days. The rats were weighed and bled daily and in one experiment were housed in metabolic cages and urine was collected. 2. Des-(1–3)-insulin-like growth factor-1 caused a lower and earlier peak in both serum creatinine and blood urea-nitrogen levels, and a more rapid and complete return toward basal values than in untreated animals. Also des-(1–3)-insulin-like growth factor-1 significantly increased creatinine clearance and reduced fractional excretion of filtered sodium. Besides these beneficial effects on kidney function, des-(1–3)-insulin-like growth factor-1 was anabolic as treated rats gained weight while control rats lost weight. The mortality in control rats was 28% compared with 6% in treated rats. 3. Thus des-(1–3)-insulin-like growth factor-1 accelerated recovery from acute ischaemic injury and may be useful for the treatment of acute renal failure.

Glycogen phosphorylase isoenzyme BB in diagnosis of myocardial ischaemic injury and infarction

1996 ◽  
pp. 289-295 ◽  
Author(s):  
Ernst-Georg Krause ◽  
Georg Rabitzsch ◽  
Franz Noll ◽  
Johannes Mair ◽  
Bernd Puschendorf
Keyword(s):  
Glycogen Phosphorylase ◽  
Ischaemic Injury
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