Changing stroke rehab and research worldwide now.Time is Brain! trillions and trillions of neurons that DIE each day because there are NO effective hyperacute therapies besides tPA(only 12% effective). I have 523 posts on hyperacute therapy, enough for researchers to spend decades proving them out. These are my personal ideas and blog on stroke rehabilitation and stroke research. Do not attempt any of these without checking with your medical provider. Unless you join me in agitating, when you need these therapies they won't be there.

What this blog is for:

My blog is not to help survivors recover, it is to have the 10 million yearly stroke survivors light fires underneath their doctors, stroke hospitals and stroke researchers to get stroke solved. 100% recovery. The stroke medical world is completely failing at that goal, they don't even have it as a goal. Shortly after getting out of the hospital and getting NO information on the process or protocols of stroke rehabilitation and recovery I started searching on the internet and found that no other survivor received useful information. This is an attempt to cover all stroke rehabilitation information that should be readily available to survivors so they can talk with informed knowledge to their medical staff. It lays out what needs to be done to get stroke survivors closer to 100% recovery. It's quite disgusting that this information is not available from every stroke association and doctors group.

Monday, July 21, 2025

Aberrant highly prokineticin 2 and its association with inflammatory indexes and functional recovery in acute ischemic stroke patients

You described something but didn't correlate how to get recovered. Useless. Research goals in stroke are survivor recovery. You're fired!

 Aberrant highly prokineticin 2 and its association with inflammatory indexes and functional recovery in acute ischemic stroke patients


Lixiao SunLixiao Sun1Yuxin FuYuxin Fu1Jiecheng YangJiecheng Yang2Xiaoli WangXiaoli Wang1Dongsheng CuiDongsheng Cui1Qiang FengQiang Feng3Xuguang SongXuguang Song1Zhe LiZhe Li1Zhuangwei WangZhuangwei Wang1Wenchao WangWenchao Wang4Yiping Wu
Yiping Wu4*Jingmei Wang
Jingmei Wang1*
  • 1Department of Critical Care Medicine, Handan Central Hospital, Handan, China
  • 2Child Care, Merice Cody Public School, Toronto, ON, Canada
  • 3Department of Cardiology, Handan Central Hospital, Handan, China
  • 4Department of Neurology, Handan Central Hospital, Handan, China

Background: Prokineticin 2 is associated with the macrophages-mediated biological process, neuronal death, oxidative stress, and inflammatory processes, while its clinical value in patients with acute ischemic stroke (AIS) has not been explored. This study aimed to evaluate the level of prokineticin 2 and its association with inflammatory indexes and functional recovery in AIS patients.

Methods: Serum samples in 210 AIS patients at admission and in 30 healthy subjects at enrollment were collected. Then, prokineticin 2 levels were determined by enzyme-linked immunosorbent assay.

Results: Prokineticin 2 level was higher in AIS patients than healthy subjects (p < 0.001). Prokineticin 2 showed an acceptable ability to distinguish the AIS patients from healthy subjects (area under the curve: 0.812) with the best cut-off value at 4 ng/mL. No matter dividing the prokineticin 2 by continuous variable or quartiles, its value was positively correlated with the high sensitivity C reactive protein (HsCRP), tumor necrosis factor-alpha (TNF-α), and interleukin 17A (IL-17A) (all p < 0.001). Prokineticin 2 showed a higher trend in AIS patients with Modified Rankin Scale (mRS) score>2 compared with those with mRS score ≤2, but without statistical significance (p = 0.095). Besides, there was no association between prokineticin 2 by quartiles and the percentage of mRS > 2 (p > 0.05).

Conclusion: Prokineticin 2 aberrantly highly expresses, and it indicates the inflammatory status, but with limited ability to predict the neural functional recovery in AIS patients.

Introduction

Acute ischemic stroke (AIS), caused by the occlusion of the cerebral artery, is a fatal central nervous system vascular event, which is one of the main reasons for death and disability for human beings worldwide (13). During the past decades, with the changes in diet and lifestyle, the incidence of AIS indicates an increased trend, and it is even as high as 13.7 million new cases per year in 2016 (46). Therefore, the treatment of AIS has drawn a lot of attention from clinicians recently. Currently, even though some progress has been made in exploring the pathogenesis and the treatment modality for AIS patients [such as thrombolytic, antithrombotic therapy, mechanical thrombectomy (MT), etc.], their prognosis still remains poor due to the short “treatment window” (712). Hence, early detection of the pathogenesis of AIS and administrating the corresponding treatment would be helpful in improving the outcomes of AIS patients.

Prokineticin 2, an 8-kD secretory protein, presents a structural similarity with peptide toxins, which has been recently reported to be associated with the macrophages-mediated biological process, neuronal death, oxidative stress, and inflammatory processes (1316). Recently, the clinical value of prokineticin 2 in the diagnosis of nervous system or inflammation-related disease and evaluation of the disease severity has been preliminary explored (1719). For instance, one study indicates that prokineticin 2 is highly expressed in Parkinson’s disease patients and serves as a biomarker in indicating gut inflammation (17). Hence, it is reasonable to hypothesize that prokineticin 2 could also be a biomarker to indicate the AIS occurrence and its inflammatory level. However, there is still a lack of evidence.

Hence, this study aimed to explore the level of prokineticin 2 and its association with inflammatory indexes and functional recovery in AIS patients.

More at link.

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