Associations of eosinophil-to-monocyte ratio and C-reactive protein-to-high-density lipoprotein cholesterol ratio with early neurological deterioration after thrombolysis in acute ischemic stroke

'Associations' DO NOTHING FOR SURVIVOR RECOVERY! Are you that blitheringly stupid you don't know that survivors would like recovery rather than a completely fucking useless 'association'? 

Had you been thinking at all you would be solving the  5 causes of the neuronal cascade of death in the first week saving hundreds of million to billions of neurons! Thus, preventing early neurological deterioration. Or don't you have two functioning neurons to rub together for a spark of intelligence?

 Associations of eosinophil-to-monocyte ratio and C-reactive protein-to-high-density lipoprotein cholesterol ratio with early neurological deterioration after thrombolysis in acute ischemic stroke

Guohua HeGuilan XuYanqiao XiaoZhen WangYachun Yu^*

• Department of Neurology, The Affiliated Changsha Central Hospital, Hengyang Medical School, University of South China, Changsha, China

Background: Inflammation mechanisms play critical roles in acute ischemic stroke (AIS). However, the correlations of the eosinophil-to-monocyte ratio (EMR) and blood C-reactive protein to high-density lipoprotein cholesterol (CRP/HDL-C) ratio with post-thrombolysis early neurological deterioration (END) in patients with AIS remain uncertain.

Methods: Patients with AIS who received intravenous thrombolysis therapy from January 2020 to February 2025 were retrospectively recruited for this study. CRP level, blood lipid concentrations, and complete blood count measurements were recorded within 24 h of admission. Post-thrombolysis END was defined as an increase in the U.S National Institutes of Health Stroke Scale (NIHSS) score of ≥ 4 points compared to the initial NIHSS score taken within 24 h of initiating intravenous thrombolysis. Multivariate logistic regression modeling was performed to evaluate the correlations of EMR and the CRP/HDL-C ratio to post-thrombolysis END. Receiver operating characteristic (ROC) curves were used to analyze the predictive value of both EMR and the CRP/HDL-C ratio in patients with post-thrombolysis END.

Results: Among 473 recruited patients, 103 (21.78%) were diagnosed with post-thrombolysis END. Patients with END had significantly higher systolic and diastolic blood pressures, white blood cell and monocyte counts, CRP levels, CRP/HDL-C ratios, and NIHSS scores on admission, while their eosinophil counts and EMRs were significantly lower. The multivariate logistic regression analysis indicated that EMR (odds ratio [OR], 0.03 [95% confidence interval (CI) 0.01–0.14]; p < 0.001) and CRP/HDL-C (odds ratio, 1.04[95%CI 1.01–1.08]; p = 0.025) were independently associated with END after adjusting for potential confounders. The areas under the receiver operating characteristic curve (AUC) for EMR and the CRP/HDL-C ratio were 0.757 (95% CI, 0.709–0.805) and 0.61 (95% CI, 0.545–0.675), respectively.

Conclusion: A lower EMR level and a higher CRP/HDL-C ratio in patients with AIS are independently associated with post-thrombolysis END. EMR and the CRP/HDL-C ratio may be potential biomarkers for post-thrombolysis END.

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Age-related impairments reversed in animal model

Your doctor will do just as well with this as with the young blood rejuvenation. And EXACTLY WHAT DID YOUR DOCTOR DO WITH YOUNG BLOOD? NOTHING? Good, you can expect nothing to ever get from research to an intervention. If you have no hope, then you will never be disappointed. 

Young Blood Revitalizes the Aging Brain June 2014 

The latest here:

Age-related impairments reversed in animal model

ScienceDaily Top Science|July 7, 2020

Frailty and immune decline are two main features of old age. Researchers from the University of Bern and the University Hospital Bern now demonstrate in an animal model that these two age-related impairments can be halted and even partially reversed using a novel cell-based therapeutic approach.

Elderly people are more prone to infectious diseases as the function of their immune system continuously declines with progression of age. This becomes especially apparent during seasonal influenza outbreaks or the occurrence of other viral diseases such as COVID-19. As the efficacy of vaccination in the elderly is strongly reduced, this age group is particularly vulnerable to such infectious pathogens and often shows the highest mortality rate. In addition to the age-related immune decline aged individuals are commonly affected by frailty that negatively impacts quality-of-life. Even though the average life-expectancy for humans continuous to rise, living longer is often associated with age-related health issues.

Important role of belly fat in aging processes identified

Researchers from the Department for BioMedical Reserarch (DBMR) and the Institute of Pathology at the University of Bern as well as the University Hospital Bern (Inselspital) have set out to identify new approaches to improve health-span in a fast-growing aging population. For many years scientists speculated that chronic low-grade inflammation accelerates aging processes and the development of age-related disorders. An international team of researchers under Bernese guidance has now demonstrated that visceral adipose tissue, known as belly fat, crucially contributes to the development of chronic low-grade inflammation. Scientist around Dr. Mario Noti, formerly at the Institute of Pathology of the University of Bern and Dr. Alexander Eggel from the Department for BioMedical Research (DBMR) of the Universität of Bern reported that certain immune cells in the belly fat play and an essential role in regulating chronic low-grade inflammation and downstream aging processes. They could show, that these immune cells may be used to reverse such processes. The findings of this study have been published in the scientific journal Nature Metabolism and were further highlighted by a News and Views editorial article.

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Belly fat as a source of chronic inflammation

The team around Dr. Noti and Dr. Eggel could demonstrated that a certain kind of immune cells, known as eosinophils, which are predominantly found in the blood circulation, are also present in belly fat of both humans and mice. Although classically known to provide protection from parasite infection and to promote allergic airway disease, eosinophils located in belly fat are responsible to maintain local immune homeostasis. With increasing age the frequency of eosinophils in belly fat declines, while the number of pro-inflammatory macrophages increases. Owing to this immune cell dysbalance, belly fat turns into a source of pro-inflammatory mediators accumulating systemically in old age.

Eosinophil cell therapy promotes rejuvenation

In a next step, the researchers investigated the possibility to reverse age-related impairments by restoring the immune cell balance in visceral adipose tissue. "In different experimental approaches, we were able to show that transfers of eosinophils from young mice into aged recipients resolved not only local but also systemic low-grade inflammation," says Dr. Eggel. "In these experiments, we observed that transferred eosinophils were selectively homing into adipose tissue," adds Dr. Noti. This approach had a rejuvenating effect on the aged organism. As a consequence, aged animals showed significant improvements in physical fitness as assessed by endurance and grip strength tests. Moreover, the therapy had a rejuvenating effect on the immune system manifesting in improved vaccination responses of aged mice.

Translating findings into clinics

"Our results indicate that the biological processes of aging and the associated functional impairments are more plastic than previously assumed," states Dr. Noti. Importantly, the observed age-related changes in adipose immune cell distribution in mice were also confirmed in humans. "A future direction of our research will be to now leverage the gained knowledge for the establishment of targeted therapeutic approaches to promote and sustain healthy aging in humans," says Dr. Eggel.

This study has been supported by the VELUX STIFTUNG, the FONDATION ACTERIA, and funds of the FreeNovation and medical-biological science research programs of Novartis.

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