scholarly journals Interleukin-6: A Novel Target for Cardio-Cerebrovascular Diseases

2021 ◽  
Vol 12 ◽  
Author(s):  
Jian-Hui Su ◽  
Meng-Yi Luo ◽  
Na- Liang ◽  
Shao-Xin Gong ◽  
Wei Chen ◽  
...  
Keyword(s):  
Cerebrovascular Disease ◽  
Interleukin 6 ◽  
Cerebrovascular Diseases ◽  
Cerebral Injury ◽  
Inflammatory Factors ◽  
Cerebrovascular Event ◽  
Novel Target ◽  
Novel Strategy ◽  
The Stability ◽  
Infarction Heart

Cardio-Cerebrovascular Disease is a collective term for cardiovascular disease and cerebrovascular disease, being a serious threat to human health. A growing number of studies have proved that the content of inflammatory factors or mediators determines the stability of vascular plaque and the incidence of cardio-cerebrovascular event, and involves in the process of Cardio-Cerebrovascular Diseases. Interleukin-6 is a widely used cytokine that causes inflammation and oxidative stress, which would further result in cardiac and cerebral injury. The increased expression of interleukin-6 is closely related to atherosclerosis, myocardial infarction, heart failure and ischemic stroke. It is a key risk factor for these diseases by triggering inflammatory reaction and inducing other molecules release. Therefore, interleukin-6 may become a potential target for Cardio-Cerebrovascular Diseases in the future. This paper is aimed to discuss the expression changes and pathological mechanisms of interleukin-6 in Cardio-Cerebrovascular Diseases, and to provide a novel strategy for the prevention and treatment of Cardio-Cerebrovascular Diseases.

The degree of severity and structure of cognitive disorders in patients with cerebrovascular disease, depending on the level of 25-hydroxycalciferol

2021 ◽  
Vol 21 (2) ◽  
pp. 53-61
Author(s):  
Gregory I. Shvartsman ◽  
Evgeniya M. Pervova ◽  
Vitaly V. Goldobin ◽  
Natalia M. Tertyshnaya
Keyword(s):  
Cerebrovascular Disease ◽  
Interleukin 6 ◽  
Peripheral Blood ◽  
Comparison Group ◽  
Neuropsychological Testing ◽  
Cognitive Disorders ◽  
Inflammatory Factors ◽  
Delayed Reproduction ◽  
Highly Sensitive ◽  
And Gender

BACKGROUND: In recent years, a significant increase in cerebrovascular pathology, which is often accompanied by cognitive deficits, has been noted all over the world. AIM: The aim of this study is to determine the severity and structure of cognitive disorders depending on the level of 25(OH)D in patients with cerebrovascular disease. MATERIALS AND METHODS: 146 patients with cerebrovascular disease aged from 30 to 80 years were examined. The comparison group consisted of 40 patients, comparable in age and gender, without the studied pathology. During the study, the level of 25(OH)D, interleukin-6, highly sensitive C-reactive protein in the peripheral blood was determined in patients and a neuropsychological examination was performed. RESULTS: In patients with cerebrovascular disease, the level of 25(OH)D it was lower in comparison with patients without this pathology. Patients with higher rates of inflammatory factors had significantly lower concentrations of 25(OH)D in the peripheral blood. The study revealed a correlation between the level of 25(OH)D in peripheral blood and the results of neuropsychological testing: direct MMSE, MoCA, FAB and reverse Schulte tables (performance). When assessing cognitive disorders in patients with cerebrovascular disease, according to the results of neuropsychological testing, it was possible to identify significantly significant differences between the main and the comparison group according to the following scales: MMSE (p = 0.04), MoCA (p = 0.001), FAB (p = 0.007), Schulte Tables (performance) (p = 0.06), respectively. When interpreting the MMSE scale, significantly significant differences between the groups were found in the attention assessment (p = 0.03), and in the analysis of the MoCA scale in the sections delayed reproduction (p = 0.03) and conceptualization (p = 0.04), respectively. In patients with cerebrovascular disease, memory is most affected by the type of delayed reproduction failure, which was observed in 53-76% of cases in our study. CONCLUSIONS: The study found that the higher the concentration of 25(OH)D and the lower the level of interleukin-6 and highly sensitive CRP in the peripheral blood, the less likely it is to develop cognitive disorders. In patients with cerebrovascular disease, memory is most affected by the type of delayed reproduction failure.

Arg506GIn Factor V Mutation (Factor V Leiden) in Patients with Ischaemic Cerebrovascular Disease and Survivors of Myocardial Infarction

1995 ◽  
Vol 73 (04) ◽  
pp. 558-560 ◽  
Author(s):  
Kimmo Kontula ◽  
Antti Ylikorkala ◽  
Helena Miettinen ◽  
Alpo Vuorio ◽  
Ritva Kauppinen-Mäkelin ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Cerebrovascular Disease ◽  
Factor V Leiden ◽  
Mutant Gene ◽  
Arterial Disease ◽  
Cerebrovascular Diseases ◽  
Extensive Study ◽  
Carrier Status ◽  
Factor V ◽  
Ischaemic Attack

SummaryThe point mutation Arg506->Gln of factor V was recently shown to be an important and relatively common genetic cause of venous thromboembolism. Using a DNA technique based on polymerase chain reaction, we surveyed the blood samples of 236 patients with ischaemic stroke or a transient ischaemic attack, 122 survivors of myocardial infarction and 137 control subjects for the presence of this mutation. Although the frequency of the factor V mutation in patients with arterial disease (4.5%) was not significantly different from that in healthy blood donors (2.9%), a carrier status for this mutant gene was associated with symptoms of migraine and relatively mild angiographic abnormalities among patients with cerebrovascular disease. A more extensive study addressing the occurrence and significance of the mutant factor V mutation in patients with vasospastic cerebrovascular diseases seems to be warranted.

Specialized, pro-resolving mediators as potential therapeutic agents for alleviating fibromyalgia symptomatology

Pain Medicine ◽  
2021 ◽  
Author(s):  
Gregory Livshits ◽  
Alexander Kalinkovich
Keyword(s):  
Animal Experiments ◽  
Therapeutic Agents ◽  
Treatment Modalities ◽  
Inflammatory Factors ◽  
Gut Dysbiosis ◽  
Unsuccessful Treatment ◽  
Pain Sensitization ◽  
Novel Strategy ◽  
Inflammation Resolution

Abstract Objective To present a hypothesis on a novel strategy in the treatment of fibromyalgia (FM). Design A narrative review. Setting FM as a disease remains a challenging concept for numerous reasons, including undefined etiopathogenesis, unclear triggers and unsuccessful treatment modalities. We hypothesize that the inflammatome, the entire set of molecules involved in inflammation, acting as a common pathophysiological instrument of gut dysbiosis, sarcopenia, and neuroinflammation, is one of the major mechanisms underlying FM pathogenesis. In this setup, dysbiosis is proposed as the primary trigger of the inflammatome, sarcopenia as the peripheral nociceptive source, and neuroinflammation as the central mechanism of pain sensitization, transmission and symptomatology of FM. Whereas neuroinflammation is highly-considered as a critical deleterious element in FM pathogenesis, the presumed pathogenic roles of sarcopenia and systemic inflammation remain controversial. Nevertheless, sarcopenia-associated processes and dysbiosis have been recently detected in FM individuals. The prevalence of pro-inflammatory factors in the cerebrospinal fluid and blood has been repeatedly observed in FM individuals, supporting an idea on the role of inflammatome in FM pathogenesis. As such, failed inflammation resolution might be one of the underlying pathogenic mechanisms. In accordance, the application of specialized, inflammation pro-resolving mediators (SPMs) seems most suitable for this goal. Conclusions The capability of various SPMs to prevent and attenuate pain has been repeatedly demonstrated in laboratory animal experiments. Since SPMs suppress inflammation in a manner that does not compromise host defense, they could be attractive and safe candidates for the alleviation of FM symptomatology, probably in combination with anti-dysbiotic medicine.

Abstract TP165: Cardiac Screening Does not Improve One-year Mortality Among Patients With Cerebrovascular Disease

Stroke ◽  
2016 ◽  
Vol 47 (suppl_1) ◽  
Author(s):  
Jason J Sico ◽  
Fitsum Baye ◽  
Laura J Myers ◽  
John Concato ◽  
Linda S Williams ◽  
...  
Keyword(s):  
High Risk ◽  
Cerebrovascular Disease ◽  
Stress Testing ◽  
Cerebrovascular Event ◽  
Mortality Benefit ◽  
Cardiac Stress ◽  
Cardiac Screening ◽  
All Cause Mortality ◽  
Cardiac Stress Testing ◽  
One Year

Introduction: Guidelines recommend the use of cardiac stress testing to screen for occult coronary heart disease (CHD) among patients with ischemic stroke/TIA who have a ‘high risk’ Framingham Cardiac Risk score (FCRS). It is unclear whether implementation of this guideline confers a mortality benefit among patients with cerebrovascular disease. Hypothesis: We assessed the hypothesis that cardiac stress testing would be associated with lower odds of one-year all-cause mortality. Methods: Administrative data from a sample of 11,306 Veterans admitted to 134 Veterans Health Administration (VHA) facilities with a stroke or TIA in fiscal year 2011 were analyzed. Patients were excluded (n=6915) on the basis of: prior CHD history, receipt of cardiac stress testing within 18-months prior to cerebrovascular event, death within 90 days of discharge, being discharged to hospice, transferred to a non-VHA acute care facility, or missing/unknown race. A FCRS was calculated for each patient; a score of ≥ 20% was classified as ‘high risk’ of having CHD. Administrative data were used to identify whether cardiac stress testing was performed within 90-days after the cerebrovascular event. Logistic regression was used to assess whether cardiac stress testing was associated with one-year all-cause mortality. Results: Of the 4391 eligible patients, 62.8% (2759) had FCRS ≥ 20%, with 4.5% (n=123) of these patients receiving cardiac stress testing within 90 days of discharge. After adjusting for sociodemographic characteristics and medical comorbidities, FCRS ≥ 20% was associated with one-year mortality (aOR=2.18; CI 95 :1.59, 3.00), however, receipt of stress testing was not (aOR=0.59; CI 95 :0.26, 1.30). Conclusion: Cardiac screening did not confer a one-year all-cause mortality benefit among patients with cerebrovascular disease. Additional work is needed to assess outcomes among patients with cerebrovascular disease who are at ‘high risk’ for CHD.

scholarly journals Association between Atmospheric Particulate Pollutants and Mortality for Cardio-Cerebrovascular Diseases in Chinese Korean Population: A Case-Crossover Study

2018 ◽  
Vol 15 (12) ◽  
pp. 2835 ◽  
Author(s):  
Chao Zhang ◽  
Zhenyu Quan ◽  
Qincheng Wu ◽  
Zhezhen Jin ◽  
Joseph Lee ◽  
...  
Keyword(s):  
Air Pollution ◽  
Cerebrovascular Disease ◽  
Cerebrovascular Diseases ◽  
Air Pollutant ◽  
Aerodynamic Diameter ◽  
Case Crossover ◽  
Disease Mortality ◽  
Particulate Pollutants ◽  
Pm2.5 And Pm10 ◽  
The Relationship

Background: Air pollution in large Chinese cities has led to recent studies that highlighted the relationship between particulate matters (PM) and elevated risk of cardio-cerebrovascular mortality. However, it is unclear as to whether: (1) The same adverse relations exist in cities with relatively low levels of air pollution; and (2) the relationship between the two are similar across ethnic groups. Methods: We collected data of PM2.5 (PM with an aerodynamic diameter ≤ 2.5 µm) and PM10 (aerodynamic diameter ≤ 10 µm) in the Yanbian Korean Autonomous Prefecture between 1 January 2015 and 31 December 2016. Using a time-stratified case-crossover design, we investigated whether levels of particulate pollutants influence the risk of cardio-cerebrovascular disease mortality among ethnic Korean vs. ethnic Han residents residing in the Yanbian Korean Autonomous Prefecture. Results: Under the single air pollutant model, the odds ratios (ORs) of cardio-cerebrovascular disease were 1.025 (1.024–1.026) for each 10 μg/m3 increase in PM2.5 at lag0 day, 1.012 (1.011–1.013) for each 10 μg/m3 increase in PM10 at lag1 day. In the multi-pollutant model adjusted by PM10, SO2, and NO2, the ORs of cardio-cerebrovascular disease were 1.150 (1.145–1.155) for ethnic Koreans and 1.154 (1.149–1.158) for ethnic Hans for each 10 μg/m3 increase in PM2.5. In the multi-pollutant model adjusted by PM2.5, SO2, and NO2, the ORs of cardio-cerebrovascular disease were 1.050 (1.047–1.053) for ethnic Koreans and 1.041 (1.039–1.043) for ethnic Hans for each 10 μg/m3 increase in PM10. Conclusion: This study showed that PM2.5 and PM10 were associated with increased risks of acute death events in residential cardio-cerebrovascular disease in Yanbian, China.

Study on pharmacokinetics of nimodipine nano-controlled release agent modified by host-guest reaction of β-cyclodextrin in rats

2021 ◽  
Vol 11 (6) ◽  
pp. 839-845
Author(s):  
Xiaoxiu Fu ◽  
Lin Ma ◽  
Yang Cao ◽  
Hengzhong Xu ◽  
Yan Guo
Keyword(s):  
Controlled Release ◽  
The Elderly ◽  
Rat Plasma ◽  
Cerebrovascular Diseases ◽  
Absolute Bioavailability ◽  
Release Agent ◽  
Dihydropyridine Calcium Channel Antagonist ◽  
Oral Preparation ◽  
Ischemic Cerebrovascular Diseases ◽  
The Stability

Nimodipine (NIMO) has been identified as a second-generation dihydropyridine calcium channel antagonist. NIMO’s specificity for the cerebrovascular smooth muscle contributes to its broad usage in treating ischemic cerebrovascular diseases in the elderly. Therefore, enhancing NIMO’s therapeutic effect and reducing its adverse reactions caused by short-term repeated use have become a focus of research. As a result, a new controlled-release preparation of NIMO, the carboxymethyl chitosan/nimodipine-hydroxypropyl-β-cyclodextrin nanoparticle (Nano-NIMO), was constructed based on hydroxypropyl-β-cyclodextrin. The novel composite Nano-NIMO preparation could significantly improve the stability of NIMO in rat plasma, achieving an absolute bioavailability as high as 62.3%, which is three times that of the traditional NIMO oral preparation. Therefore, Nano-NIMO is expected to provide a new direction for the preparation of modified controlled-release Nano- NIMO agents.

Abstract 3872: Transgenic HuR in Astrocytes Increases Ischemic Lesion Size in Mice

Stroke ◽  
2012 ◽  
Vol 43 (suppl_1) ◽  
Author(s):  
Randall S Carpenter ◽  
Cyrus L Hinkson ◽  
Peter H King ◽  
Agnieszka A Ardelt
Keyword(s):  
Cerebral Ischemia ◽  
Mrna Stability ◽  
Lesion Size ◽  
Artery Occlusion ◽  
Translational Efficiency ◽  
Test Analysis ◽  
Ischemic Lesion ◽  
Term Survival ◽  
Novel Target ◽  
The Stability

Introduction: Stroke is a serious neurological disorder that affects more than 800,000 Americans each year. HuR, an mRNA binding protein, regulates gene expression by modulating the stability and translational efficiency of mRNAs containing adenine-uridine rich elements in the 3’ untranslated region. Genes implicated in neuroprotection and post-ischemic repair may be regulated by HuR. The current investigation utilizes transgenic mice engineered to express Flag-HuR in astrocytes using the glial fibrillary acidic protein (GFAP) promoter. We hypothesized that modulation of mRNA stability in astrocytes would change the outcome from transient cerebral ischemia. Methods: Four mouse cohorts were studied: male or female and transgenic (TG) or wild-type (WT). Mice underwent 30-minute transient right middle cerebral artery occlusion (MCAO) and survived for 24 or 72h. Neurological scores were recorded after ischemia and prior to euthanasia, and brain tissue was sectioned for histology and immunolabeling. In a blinded fashion, Flag-HuR expressing nuclei were counted in peri-lesional regions of interest (ROI) and contralateral mirror ROIs, and ischemic/contralateral indices were calculated. Representative lesion size was determined in hematoxylin-eosin sections at the level of Bregma 1.10 mm. Results:HuR-Flag expression: The transgene was expressed in peri-lesional astrocytes. 24h after MCAO, hormonally intact female mice had higher levels of Flag-HuR expression: Flag-HuR index was 5.9 ± 1.9 in females (n = 7) vs. 2.0 ± 0.7 in males (n = 6), p = 0.002, Mann-Whitney rank sum test. 72h after MCAO, TG expression declined in females to levels comparable to those of males. Lesion size: There was no difference in lesion size between sex-matched TG and WT mice 24h post-MCAO, but at 72h lesion size was larger in TG females than WT females: 47% ± 12 (n = 10) vs. 22% ± 11 (n = 5), respectively, p = 0.002, t-test. Analysis of neurological scores, sex hormone levels, and long term survival is ongoing. Discussion: We hypothesized that altering mRNA stability in ischemic astrocytes would change outcome from cerebral ischemia. Initial characterization of TG mice in which HuR was expressed under control of the GFAP promoter showed that ischemia results in peri-lesional upregulation of the transgene, which is more robust in females than males 24h after MCAO and comparable to males 72h after MCAO. Transgene expression correlated with increased lesion size in females 72h after MCAO. While the mechanism of this effect requires elucidation, our results suggest that HuR is a viable novel target for further investigation in cerebral ischemia.

Cardiac Troponin I Microfluidic Chip Driven by Adaptive Pressure

2020 ◽  
Vol 12 (10) ◽  
pp. 1239-1247
Author(s):  
Xingshang Xu ◽  
Yuan Liu ◽  
Zhu Chen ◽  
Hui Chen ◽  
Yan Deng ◽  
...  
Keyword(s):  
Microfluidic Chip ◽  
Whole Blood ◽  
Cardiac Troponin ◽  
Troponin I ◽  
Accurate Determination ◽  
Cardiac Troponin I ◽  
Chip Surface ◽  
Layer Composite ◽  
Novel Strategy ◽  
The Stability

To develop and design an adaptive microfluidic chip for accurate determination of cardiac troponin I (cTnI) in whole blood sample and explore the operating parameters of the chip in detecting cTnI, in order to provide a novel strategy for the detection of cTnI, cTnI microfluidic chip was prepared by injection moulding, and the improved polystyrene polymer was used as the chip substrate to construct a three-layer composite structure, namely the upper, middle, and lower layers. The antihuman troponin I antibody I/II was grafted onto the chip surface to construct the detection reaction zone using UV-induced production of surface-active free radicals. The stability of the chip preparation process, the running performance of the chip, and the analytical performance of the whole blood samples were investigated. It was shown that I adaptive pressure-driven microfluidic chip has the advantages of easy bonding, integration, and a simple and stable production process. In the actual detection and analysis, the chip has high selectivity for cTnI in whole blood, lower detection limit (0.054 ng/mL), and small difference between batches (RSD% 2.50%). Therefore, the chip is assumed to provide novel strategy for the assessment of myocardial infarction by detecting cTnI.

SP495TARGETING INTERLEUKIN 6 AND INTERLEUKIN 8: A NOVEL STRATEGY FOR PREVENTING THE PROGRESSION OF PERITONEAL CALCIFICATION

2019 ◽  
Vol 34 (Supplement_1) ◽  
Author(s):  
Tzu-Ming Jao ◽  
Chia-Ter Chao ◽  
Chih-Kang Chiang ◽  
Jenq-Wen Huang ◽  
Kuan-Yu Hung
Keyword(s):  
Interleukin 6 ◽  
Interleukin 8 ◽  
Novel Strategy

scholarly journals Improved detection of cerebrovascular disease processes: Introduction to the Journal of Cerebral Blood Flow and Metabolism special issue on cerebrovascular disease

2018 ◽  
Vol 38 (9) ◽  
pp. 1387-1390 ◽  
Author(s):  
Manus J Donahue ◽  
Jeroen Hendrikse
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Cerebrovascular Disease ◽  
Developed Countries ◽  
The United States ◽  
Cerebrovascular Diseases ◽  
Stroke Recovery ◽  
Special Issue ◽  
Permanent Disability ◽  
Stroke Incidence

Approximately 15 million individuals suffer a stroke worldwide each year, and stroke results in death or permanent disability in two-thirds of these individuals. Due to increased knowledge and management of modifiable risk factors, stroke incidence in developed countries is declining, however remains high at just under 1 million patients per year in the United States alone. Further improving management of patients with cerebrovascular disease (CVD) ultimately will require development and clinical adoption of sensitive markers of hemodynamic and metabolic failure, as well as trials that evaluate how to interpret these markers to optimize therapies. Realizing this goal and reducing the complete burden of CVD is dependent on an improved understanding of the pathophysiological processes that underlie CVD in all stages, including sub-clinical disease processes, acute stroke, and post-stroke recovery mechanisms. This document serves as an introduction to the Journal of Cerebral Blood Flow and Metabolism special issue on cerebrovascular diseases, which is comprised of contributions from experts in each of the above stages of CVD, and outlines current standards for patient management and emerging directions that have potential for improving patient care over the next decade.

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