Allegheny Health Network Neurosurgeon Performs the Region's First Vagus Nerve Stimulation Procedure to Enhance Stroke Recovery

That has to be pure incompetency on the doctors and hospital! Let's see how long vagus nerve stimulation has been out there. And why not the non-invasive types?

• vagus nerve (67 posts to July 2012)

• • paired vagus nerve stimulation (2 posts to April 2022)

 Allegheny Health Network Neurosurgeon Performs the Region's First Vagus Nerve Stimulation Procedure to Enhance Stroke Recovery

Innovative Therapy Helps Wexford Stroke Survivor Regain Hand Function and

Return to Playing Guitar

B-ROLL AND INTERVIEWS:  https://f.io/lpCCNeXD

VIDEO of Vivistim® Paired VNS System: microtransponder | Showpad

PITTSBURGH, Pa., April 3, 2025 /PRNewswire/ -- Stroke is a potentially debilitating neurologic injury which affects about 800,000 Americans annually and often results in a loss of mobility and motor function. A breakthrough therapeutic technology now being offered at Allegheny Health Network's (AHN) Allegheny General Hospital (AGH) however, is offering new hope to stroke patients who have lost strength and motor control of their arms and hands.  

The Vivistim® Paired Vagus Nerve Stimulation (VNS) System is an FDA-approved technology designed to help stroke survivors regain movement in their upper extremities by delivering mild, repeated electrical pulses to the vagus nerve, which runs from the brainstem through the neck and into the body.  Research has shown that stimulating the nervous system through the vagus nerve can create new pathways in the brain, allowing the patient to regain function and strength faster than through rehabilitation alone.

Alexander Whiting, MD, neurosurgeon and director of epilepsy surgery at AHN's Neuroscience Institute, recently performed the first VNS procedures for stroke recovery in western Pennsylvania. The technology, he said, offers a new pathway to recovery for patients who have reached the limits of traditional occupational and physical therapy.

Among the first to benefit from the innovative treatment is Scott Pavlot, 66, of Wexford, Pa.

Scott, a beloved community leader and musician suffered a life-altering ischemic stroke on Feb. 12, 2024, just two days after his birthday. The stroke left him with severe impairment on his left side, including paralysis of his arm and hand, threatening his ability to continue with his life's passions — playing bass guitar and running The West View HUB, a nonprofit he founded to support the community through free arts, education, and food-assistance programs.

According to the American Stroke Association, an ischemic stroke occurs when a vessel supplying blood to the brain is obstructed. It accounts for about 87% of all strokes.

"I got a brand-new bass for my birthday and only got to play it for one day before the stroke," Scott said. "At first, I couldn't move my arm or fingers at all, but I never saw myself as disabled, just temporarily compromised. That's why I jumped at the chance to try Vivistim. I wanted to push my recovery as far as I could."

Traditionally, stroke rehabilitation focuses on repetitive movement exercises to help the brain form new neural pathways by way of its "neuroplasticity," or the brain's ability to rewire and reorganize itself. However, after about two to three months of therapy, many patients plateau, struggling to make further improvements. The Vivistim System is designed to extend and enhance that window of recovery by delivering mild electrical pulses to the vagus nerve.

The procedure involves implanting a small device, similar to a pacemaker, in the patient's chest. A thin wire is then connected from the device to the vagus nerve in the neck, which serves as a direct communication highway between the brain and body.

"The VNS implant acts like a 'turbo boost' for the brain," said Dr. Whiting. "Every time Scott engages in therapy, whether it's practicing hand exercises or playing the bass, the device stimulates his vagus nerve, sending signals to the brain that tell it to 'wake up' and rewire itself more effectively. It accelerates the natural recovery process in a way that wasn't previously possible."

Once the device is implanted, patients use a handheld magnet to activate it during rehabilitation exercises and daily activities. For Scott, this meant using the device while practicing plucking strings on his bass, helping retrain his brain to restore fine motor control in his fingers.

"This isn't just about regaining movement, it's about reclaiming independence and identity," said Dr. Whiting. "For Scott, playing music is a part of who he is. Watching him recover and pick up his bass again has been incredible."

Since receiving the Vivistim implant in September 2024, Scott has made remarkable progress. Initially, his left arm was completely paralyzed, but through consistent therapy and the help of the VNS system, he has regained movement, finger articulation, and strength.

"The difference has been huge," Scott said. "Typically, stroke recovery hits a wall after a few months. But with the VNS, I've continued to improve well beyond that point. My hand control is getting stronger, and best of all — I can play music again."

The Vivistim System is a game-changer for stroke survivors who have not regained full hand and arm function. According to the American Stoke Association, stroke patients who use VNS therapy in combination with rehabilitation experience two to three times greater functional improvement than those who undergo therapy alone.

"For many stroke survivors, losing function in their hand means losing their ability to feed themselves, dress, or do the things they love," said Dr. Whiting. "With VNS therapy, we're seeing patients regain independence and hope. This is the first time we've been able to significantly change the trajectory of stroke recovery beyond the standard rehabilitation timeline."

Scott sees himself as proof that stroke recovery doesn't have to stop after a few months.

"You can't be defined by a stroke," he said. "I've always been active in my community, my faith, and my music. I laugh every day, I push myself every day, and now I have this incredible tool to help me keep improving. This isn't the end of my story — it's just a new chapter."

For more information about Vagus Nerve Stimulation for stroke recovery at Allegheny Health Network, please call 724-228-1414 and select option 2.

U−shaped association between the glycemic variability and prognosis in hemorrhagic stroke patients: a retrospective cohort study from the MIMIC-IV database

 Useless, describes a problem; provides NO solution!

U−shaped association between the glycemic variability and prognosis in hemorrhagic stroke patients: a retrospective cohort study from the MIMIC-IV database

Yuchen Liu^1†Houxin Fu^2†Yue Wang³Jingxuan Sun¹Rongting Zhang¹Yi Zhong¹Tianquan Yang¹Yong Han¹Yongjun Xiang¹Bin Yuan¹Ruxuan Zhou¹Min Chen¹Hangzhou Wang^1*

• ¹Department of Neurosurgery, Children’s Hospital of Soochow University, Suzhou, Jiangsu, China
• ²Department of Pediatric Hematology and Oncology, Children’s Hospital of Soochow University, Suzhou, Jiangsu, China
• ³Institute of Pediatric Research, Children’s Hospital of Soochow University, Suzhou, Jiangsu, China

Background: Elevated glycemic variability (GV) is commonly observed in intensive care unit (ICU) patients and has been associated with clinical outcomes. However, the relationship between GV and prognosis in ICU patients with hemorrhagic stroke (HS) remains unclear. This study aims to investigate the association between GV and short- and long-term all-cause mortality.

Methods: Clinical data for hemorrhagic stroke (HS) patients were obtained from the MIMIC-IV 3.1 database. GV was quantified using the coefficient of variation (CV), calculated as the ratio of the standard deviation to the mean blood glucose level. The association between GV and clinical outcomes was analyzed using Cox proportional hazards regression models. Additionally, restricted cubic spline (RCS) curves were employed to examine the nonlinear relationship between GV and short- and long-term all-cause mortality.

Results: A total of 2,240 ICU patients with HS were included in this study. In fully adjusted models, RCS analyses revealed a U-shaped association between the CV and both short- and long-term all-cause mortality (P for nonlinearity < 0.001 for all outcomes). Two-piecewise Cox regression models were subsequently applied to identify CV thresholds. The thresholds for all-cause mortality in ICU, during hospitalization, and at 30, 90, and 180 days were determined to be 0.14, 0.16, 0.155, 0.14, and 0.14, respectively. These findings were consistent in sensitivity and subgroup analyses.

Conclusions: In HS patients, higher GV is associated with an increased risk of both short- and long-term all-cause mortality. Our findings suggest that stabilizing GV may improve the prognosis of HS patients.(Where the fuck is the protocol that does that? Your mentors and senior researchers need to be fired for incompetency?)

Background

Cerebrovascular disease (CVD) is the second leading cause of death worldwide, surpassed only by cardiovascular disease (1–3). Stroke, a major component of CVD, has been identified by the World Health Organization as the primary cause of long-term disability globally (4, 5). Although hemorrhagic stroke (HS) accounts for only 10–20% of all stroke cases, it is responsible for nearly half of all stroke-related deaths (6, 7). With an aging global population, the burden of stroke continues to rise, with HS patients in intensive care units (ICU) facing an elevated mortality risk (8). Consequently, identifying prognostic markers for predicting adverse outcomes in HS patients is essential. Historically, assessment tools such as the NIH Stroke Scale and the Canadian Neurological Scale have been widely utilized (9). Despite their utility, these scales are limited by their complexity, time requirements, and the need for specialized training.

Recently, glycemic variability (GV), a parameter of glycemic control, has emerged as a potential factor influencing the progression of cardiovascular and cerebrovascular conditions (10–13). GV reflects fluctuations in blood glucose levels relative to the mean and represents a key pattern of glycemic dysregulation observed in critically ill patients. Compared to persistent hyperglycemia, pronounced glycemic variability has been demonstrated to exacerbate endothelial dysfunction and trigger oxidative stress, potentially leading to more severe cerebrovascular damage (14–16). Moreover, both hyperglycemia and hypoglycemia were recognized as significant factors influencing stroke prognosis (16). Despite this, the impact of glycemic variability on HS patients has been understudied and remains a topic of debate in clinical practice (17, 18).

To address this gap, the present study examined the association between glycemic variability and short-term and long-term all-cause mortality in HS patients. The findings aimed to support clinicians in identifying high-risk individuals, facilitating closer monitoring and timely therapeutic interventions.

More at link.

Return to Work After Ischemic Stroke in Young Adults: A Multicenter Cohort Study, Systematic Review, and Meta‐Analysis

 And the blame for this problem lies directly on our stroke medical 'professionals' not creating 100% recovery protocols!

Return to Work After Ischemic Stroke in Young Adults: A Multicenter Cohort Study, Systematic Review, and Meta‐Analysis

Gabriel Yi Ren Kwok https://orcid.org/0000-0001-6849-6098, Nicole Yeong, Michelle Law, Zi Lun Kang, Arjun Achar, Xin Yuan Lim https://orcid.org/0000-0001-5088-8130, Megan B. J. Ng, BSc https://orcid.org/0000-0002-1196-6164, … Show All … , and Benjamin Y. Q. Tan, MBBS, MCI https://orcid.org/0000-0003-1824-9077 ben.tan@nus.edu.sgAuthor Info & Affiliations

Journal of the American Heart Association

New online

https://doi.org/10.1161/JAHA.124.036427

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Abstract

Background

Ischemic stroke incidence in young adults is increasing globally, with return to work (RTW) a key rehabilitation goal. We aimed to assess the overall proportions of and factors associated with RTW following young adult ischemic stroke.

Methods and Results

We performed a retrospective cohort study of all patients with ischemic stroke aged 18 to 50 years at 2 tertiary hospitals in Singapore from 2020 to 2022. We evaluated associations between patient characteristics and 3‐month RTW status, augmenting these findings with a systematic review and meta‐analysis of PubMed, Embase, Scopus, and Cochrane databases from January 2000 to November 2023. We pooled proportions for RTW and functional recovery (defined as a 90‐day modified Rankin Scale score of 0–2) and meta‐analyzed associations between patient characteristics and RTW using random‐effects models. In this multicenter cohort, 68.8% (249/362) of young patients with ischemic stroke returned to work, while 87.8% (318/362) achieved functional recovery. Multivariable logistic regression showed that patients with large‐artery atherosclerosis pathogenesis, diabetes, higher admission National Institutes of Health Stroke Scale scores, and higher 90‐day modified Rankin Scale had significantly lower odds of RTW. The systematic review and meta‐analyses of 1914 patients across 6 cohort studies identified significantly lower odds of RTW in patients with large‐artery atherosclerosis, diabetes, and admission National Institutes of Health Stroke Scale SCORE >15. The pooled proportion of RTW was 63.2% (984/1574 [95% CI, 56.0–69.9]) and functional recovery 84.7% (719/846 [95% CI, 81.1–87.8]).

Conclusions

Patients with large‐artery atherosclerosis, diabetes, and higher admission National Institutes of Health Stroke Scale score at baseline are less likely to RTW. While lower 90‐day modified Rankin Scale is significantly associated with RTW, many patients achieving functional recovery do not RTW. Well‐designed cohort studies are warranted to explore this disparity.(Exploring is not needed you BLITHERING IDIOTS! YOU CREATE 100% RECOVERY PROTOCOLS! ARE YOU THAT FUCKING STUPID?)

Effects of Intensive Blood Pressure Lowering on Brain Swelling in Thrombolyzed Acute Ischemic Stroke: The ENCHANTED Results

 

 WHOM is going to create protocols based on all this earlier research?  SPECIFIC NAMES ONLY, none of this general  crapola of followup should occur.  If your doctor and stroke hospital can't provide a specific name, THEY NEED TO BE FIRED.  I take no prisoners in trying to solve stroke, that means your doctors and PhDers need to do their job. 100% stroke recovery for all. NO EXCUSES.  

Did your stroke hospital do ANYTHING AT ALL with this earlier research? Or were they incompetent like usual?

Our laboratory has now shown that substance P is released during stroke. And blocking substance P receptors following stroke subsequently reduces brain swelling and improves outcome and survival in rats May 2012 

 

Radically New Patented Technology Highly Effective In Reducing Cerebral Oedema May 2012 

 

Discovery paves way for treatments to prevent brain damage or death following head trauma April 2015 

 

Innovative treatment may help prevent brain swelling, death in stroke patients April 2016 

 

New biodegradable pressure sensor could help monitor serious health conditions

January 2018

 

Injected Nanoparticles May Provide First Real Treatment for Traumatic Brain Injury  January 2020

Because our incompetent stroke medical 'professionals' still haven't figured out an EXACT BLOOD PRESSURE MANAGEMENT PROTOCOL post stroke! And YOU bear the failure of that! Hope your competent? doctor guesses correctly because the poor outcome happens to you! Your doctor gets off scot-free and still gets paid! My non-medical thinking on this is that by doing this you are vastly lowering the oxygen supply to the brain thus hastening the neuronal cascade of death!

• blood pressure management (90 posts to June 2017)

The latest here, once again describing a problem but PROVIDING NO SOLUTION! How incompetent can you be and still employed in stroke?

Effects of Intensive Blood Pressure Lowering on Brain Swelling in Thrombolyzed Acute Ischemic Stroke: The ENCHANTED Results

Guobin Zhang, MD, Chen Chen, MD, PhD https://orcid.org/0000-0002-8960-8797, Xinwen Ren, MPH https://orcid.org/0000-0002-5235-894X, Yang Zhao, PhD, Menglu Ouyang, PhD https://orcid.org/0000-0001-7917-6858, Laurent Billot, MRes https://orcid.org/0000-0002-4975-9793, Qiang Li, Mbiostat, … Show All … for the ENCHANTED (Enhanced Control of Hypertension and Thrombolysis Stroke Study) InvestigatorsAuthor Info & Affiliations

Stroke

New online

https://doi.org/10.1161/STROKEAHA.124.049938

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Abstract

BACKGROUND:

Cerebral swelling in relation to cytotoxic edema is a predictor of poor outcome in acute ischemic stroke (AIS) and elevated blood pressure (BP) promotes its development. Whether intensive BP-lowering treatment reduces cerebral swelling is uncertain. We aimed to determine whether intensive BP lowering reduces the severity of cerebral swelling after thrombolysis for AIS.

METHODS:

A secondary analysis of the ENCHANTED (Enhanced Control of Hypertension and Thrombolysis Stroke Study), a partial factorial, international, multicenter, open-label, blinded end point, randomized controlled trial of alteplase dose and levels of BP control in thrombolyzed patients with AIS. Participants were randomly assigned to intensive (systolic target 130–140 mm Hg within 1 hour; maintained for 72 hours) or guideline-recommended (systolic target <180 mm Hg) BP management. Available serial brain images (baseline and follow-up, computed tomography, or magnetic resonance imaging) were centrally analyzed with standardized techniques (Apollo MIStar software) by expert readers blind to clinical details to rate swelling severity (from 0 no to 6 most severe swelling [midline shift and effacement of basal cisterns]) and other abnormalities. Primary outcome was any cerebral swelling (score, 1–6) in logistic regression models.

RESULTS:

Of 1477/2196 (67.3%) patients (mean age, 67.7 years; female, 39.6%) with sequential scans, the between-group mean systolic BP difference was 6.6 mm Hg over 24 hours. No significant difference was found in the treatment effect on any cerebral swelling between intensive and guideline-recommended BP management (22.12% versus 22.39%, adjusted odds ratio, 1.05 [95% CI, 0.81–1.36]; P=0.71). Results were consistent across different groups of swelling severity (swelling score 2–6, 3–6, and 4–6; and ordinal shift on swelling score).

CONCLUSIONS:

Modest early intensive BP lowering does not seem to alter cerebral swelling in thrombolyzed patients with AIS. Further research is needed to quantify brain edema to allow a better understanding of the complex relations of BP and outcomes from AIS.

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Study finds nearly five-fold increase in hospitalizations for common cause of stroke

 

Really disappointed they excluded recent head/neck trauma like chiropractic adjustments or beauty parlor strokes.

Here's a lot more information on cervical artery dissections including precisely why you never get your neck adjusted.

cervical artery dissection (9 posts to November 2013)

Study finds nearly five-fold increase in hospitalizations for common cause of stroke

Date:

April 2, 2025

Source:

American Academy of Neurology

Summary:

Cervical artery dissection is a tear in an artery in the neck that provides blood flow to the brain. Such a tear can result in blood clots that cause stroke. A new study has found almost a five-fold increase in the number of U.S. hospitalizations for cervical artery dissection over a 15-year period.

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FULL STORY

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Cervical artery dissection is a tear in an artery in the neck that provides blood flow to the brain. Such a tear can result in blood clots that cause stroke. A new study has found almost a five-fold increase in the number of U.S. hospitalizations for cervical artery dissection over a 15-year period. The study is published on April 2, 2025, online in Neurology^®, the medical journal of the American Academy of Neurology (AAN).

A dissection in the artery wall is most often caused by trauma due to motor vehicle accidents but can also occur with smaller injuries.

Heavy lifting has also been shown to cause dissection in some people.

17 modifiable risk factors shared by stroke, dementia, and late-life depression

Because of lazy research like this we never get research that will prevent dementia EXACTLY AND BRING STROKE SURVIVORS BACK TO 100% RECOVERY. Those topics are much harder to solve and why not just write an easy piece and get published? If we had ANY LEADERSHIP AT ALL, both problems could be solved!

Closer to the actual research here: but still not telling us the 17 factors.

Modifiable Risk Factors for Stroke, Dementia, and Late-Life Depression: A Systematic Review and DALY Weighted Risk Factors for a Composite Outcome

The latest here:

17 modifiable risk factors shared by stroke, dementia, and late-life depression

Date:

April 3, 2025

Source:

Mass General Brigham

Summary:

In a new extensive systematic review, researchers identified 17 modifiable risk factors that are shared by stroke, dementia, and late-life depression. Modifying any one of them can reduce your risk of all three conditions. The findings provide evidence to inform novel tools such as the Brain Care Score.

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FULL STORY

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Age-related brain diseases such as stroke, dementia, and late-life depression are a debilitating part of growing older, but people can lower their risk of these diseases through behavioral and lifestyle changes. In a new extensive systematic review, Mass General Brigham researchers identified 17 modifiable risk factors that are shared by stroke, dementia, and late-life depression. Modifying any one of them can reduce your risk of all three conditions. The findings, which provide evidence to inform novel tools, such as the Brain Care Score, are published in the Journal of Neurology, Neurosurgery, and Psychiatry.

"Our study identified 17 modifiable risk factors shared between stroke, dementia, and/or late-life depression, emphasizing that there are many different steps individuals can take to lower their risks for these age-related brain diseases," said senior author Sanjula Singh, MD, PhD, MSc (Oxon), principal investigator at the Brain Care Labs at Massachusetts General Hospital (MGH), a founding member of the Mass General Brigham healthcare system

High Repetition Activity in Stroke Rehabilitation

 You really do know ABSOLUTELY NOTHING ABOUT STROKE RECOVERY, DO YOU? Nothing about motivation or why you don't want to do high intensity training!

My conclusion is you don't understand ONE GODDAMN THING ABOUT SURVIVOR MOTIVATION/ENGAGEMENT, DO YOU? You create EXACT 100% recovery protocols and your survivor will be motivated to do the millions of reps needed because they are looking forward to 100% recovery. GET THERE!

Your competent? doctor WILL 100% GUARANTEE that HIT(High intensity training) will not cause a stroke? By verifying that your aneurysms will not blow out? Not just pooh poohing your question?

Do you really want to do high intensity training?

Because Andrew Marr blames high-intensity training for his stroke. 

Can too much exercise cause a stroke?

The latest here:

High Repetition Activity in Stroke Rehabilitation

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https://doi.org/10.1016/j.apmr.2025.01.230

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Objectives

To investigate the effect of a high-repetition active motion home program in stroke rehabilitation.

Design

Institutional review board–approved case series with ten stroke survivor participants, at least 3 months poststroke. The in-clinic visits included pre and postintervention tests, training of device use, and a 2-week home-based intervention.

Setting

Outpatient therapy services clinic for testing and training and home setting for intervention.

Participants

All participants provided written informed consent per the institutional review board. Inclusion and exclusion criteria was used for selection of ten observational stroke survivor participants, at least 3 months poststroke. Referral was from Johns Hopkins physicians and outpatient therapy clinicians.

Interventions

Pre and postintervention arm function were measured in-clinic using the Action Research Arm Test (ARAT) and spasticity using the Modified Ashworth Scale (MAS). Participants completed a preintervention and postintervention survey on the ease of use of the device. Participants were trained in the use of the device and given a structured home-based 6 x week program including a recommended 600 reps. per day of active arm motion using the device, self-stretches, and functional use of the affected arm.

Main Outcome Measures

Arm function test using ARAT, spasticity using MAS, a preintervention and postintervention ease of device use survey, 3 postintervention open-ended questions about challenges in use of the device, adherence to the prescribed program, and motivation to use the affected arm in daily activities.

Results

The average number of repetitions achieved by each participant per day was 899.5±423. The ARAT score for arm function increased by (mean±SD) 7.1±3.9 and the MAS score for spasticity reduced by 1.0±0.6. Subjectively, there was increased reported actual the ease of use of the device postintervention compared with that anticipated preintervention; 90% of the participants reported little difficulty completing the program despite stroke- and device-related challenges and expressed increased motivation to use the arm.

Conclusions

A structured home program using high-repetition gaming devices may mitigate barriers to motivation, adherence, accessibility, and participation for stroke survivors. This study demonstrates the effect of a high-repetition active motion program at home in moderately impaired stroke survivors(So you are willing to let other survivors languish because you INCOMPETENTLY did not plan on getting them recovered?) with measurable clinically important differences in arm function and spasticity scores in a short time frame. Key ingredients include a gaming device designed for moderately impaired stroke survivors, detailed instructions on using the device, stretching, and arm use for daily activities provided by an occupational therapist.

Disclosures

none.

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Preparation and Characterization of Mitochondrial-Targeted Nitronyl Nitroxide Loaded PLGA Nanoparticles for Brain Injury Induced by Hypobaric Hypoxia in Mice

 Since low oxygen(hypoxia) occurs during stroke our non-existent stroke leaders should be creating followup research for stroke survivors. But with NO LEADERSHIP, nothing will occur. 

Preparation and Characterization of Mitochondrial-Targeted Nitronyl Nitroxide Loaded PLGA Nanoparticles for Brain Injury Induced by Hypobaric Hypoxia in Mice

Authors Da Q , Xu M, Tian Y , Ma H, Wang H, Jing L 

Received 19 November 2024

Accepted for publication 25 March 2025

Published 1 April 2025 Volume 2025:20 Pages 3999—4020

DOI https://doi.org/10.2147/IJN.S507315

Checked for plagiarism Yes

Review by Single anonymous peer review

Peer reviewer comments 2

Editor who approved publication: Professor Dong Wang

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Qingyue Da,^1,2 Min Xu,^3,4 Yiting Tian,² Huiping Ma,² Haibo Wang,³ Linlin Jing<sup>1,2

1</sup>Department of Pharmacy, The First Affiliated Hospital of Xi’an Jiaotong University, Xi’an, 710061, People’s Republic of China; ²Department of Pharmacy, The 940th Hospital of Joint Logistics Support Force of PLA, Lanzhou, Gansu, 730050, People’s Republic of China; ³Department of Chemistry, School of Pharmacy, The Air Force Medical University, Xi’an, 710032, People’s Republic of China; ⁴The Third Stationed Outpatient Department, General Hospital of Central Theater Command, Wuhan, 430070, People’s Republic of China

Correspondence: Linlin Jing, Department of Pharmacy, The First Affiliated Hospital of Xi’an Jiaotong University, No. 277 Yanta West Road, Yanta District, Xi’an, Shaanxi, 710061, People’s Republic of China, Tel +86-029-85323537, Email jinglinlin@xjtufh.edu.cn Haibo Wang, Department of Chemistry, School of Pharmacy, The Air Force Medical University, No. 169, Changle West Road, Xi’an, Shaanxi, 710032, People’s Republic of China, Tel +86-029-84774473, Email haibo7691@fmmu.edu.cn

Background: Oxidative stress is considered an important mechanism of acute high-altitude brain injury. Imidazole nitronyl nitroxide radicals are a class of stable organic radical scavengers that contain single electrons in their molecules. Therefore, in order to search for compounds with low toxicity and better effect against high-altitude brain injury, the preparation methods of PLGA nanoparticles (TPP-C₆-HPN@PLGA-NPs) loaded with a synthesized mitochondria targeting imidazole nitronyl nitroxide were emphasized and investigated. Furthermore, its protective effect on brain injury caused by low-pressure hypoxia (HH) in mice was evaluated.
Methods: Nanoparticles were prepared by emulsion solvent evaporation method, and the preparation method was optimized by Box Behnken design based on particle size, encapsulation efficiency (EE) and drug loading (DL). Physical characterization and release studies of the optimized NPs were conducted. The high altitude brain injury mice model was selected to evaluate the therapeutic effect of TPP-C₆-HPN@PLGA-NPs in vivo. The histological and biochemical tests were conducted in serum and brain of mice exposed to HH condition.
Results: The nanoparticle size was 120.63 nm, the EE was 89.30%, the DL was 6.82%, the polydispersity index (PDI) was 0.172, and the zeta potential was − 22.67 mV under optimal preparation process. In addition, TPP-C₆-HPN@PLGA-NPs owned good stabilities and sustained drug releases. TPP-C₆-HPN@PLGA-NP exhibited lower toxicity than TPP-C₆-HPN and was well uptaken by PC12 cells. Histological and biochemical analysis demonstrated that TPP-C₆-HPN@PLGA-NPs significantly reduced HH induced pathological lesions, oxidative stress, energy dysfunction and inflammation response of brain tissue. Furthermore, nanoparticles did not show significant toxicity to major organs such as the liver and kidneys, as well as hematology in mice.
Conclusion: TPP-C₆-HPN@PLGA-NPs exhibits good stability, low hemolysis rate, sustained release, low toxicity, and long residence time in brain tissue and can be used as a promising formulation for the proper treatment of HH-induced brain damage.

Keywords: nitronyl nitroxide, mitochondrial-targeted, PLGA nanoparticles, characterization, high altitude brain injury

Introduction

There is an increasing number of people, approximately 40 million or more, travelling to or visiting high-altitude (HA) areas each year.^1–3 In high-altitude areas, the decrease in oxygen partial pressure caused by low air pressure leads to a reduction in the availability of oxygen absorbed by blood and tissues, which poses a significant challenge to people’s health.⁴ The brain is particularly susceptible to damage due to hypoxia, as an organ with high metabolic and oxygen consumption rates.⁵ Drugs such as acetazolamide, dexamethasone and edaravone have demonstrated efficacy in ameliorating high-altitude hypoxia-induced brain injury (HHBI).^1,6 However, their widespread clinical adoption is significantly constrained by pronounced adverse effects. Therefore, there is currently a substantial lack of effective therapeutic approaches to HHBI.

The mechanism of acute high-altitude brain injury is relatively complex, and the reasons are not fully understood at present. Nevertheless, it is considered to involve many molecular pathways including oxidative stress (OS)⁷ and inflammation response.⁸ The state of low-pressure hypoxia can disrupt the balance between the oxidative and antioxidant systems in the brain, leading to an increase in reactive oxygen species (ROS) such as hydroxyl radicals (•OH), superoxide (O₂^•−), and hydrogen peroxide (H₂O₂), while endogenous enzyme antioxidants and non-enzyme antioxidants such as superoxide dismutase (SOD) and glutathione (GSH) decrease.⁹ Mitochondria are subcellular organelles in cells that contain DNA in addition to the nucleus. The mitochondrial respiratory chain is also the main site for ROS production. The low-pressure hypoxic environment leads to excessive production of ROS in mitochondria, causing mitochondrial damage.¹⁰

Therefore, the strategy of targeting drug delivery to mitochondria may provide a new therapeutic approach for combating HH-induced damage. So far, covalently linking drugs with lipophilic cations has been an effective method for delivering them specifically to mitochondria, for instance, linking a triphenylphosphonium (TPP) moiety to a central pharmacophore of interest.¹¹ A very successful example is Mito Q, which is covalently bonded to coenzyme Q10 by triphenylphosphate cation (TPP⁺). Studies have shown that Mito Q can effectively block the production of ROS, prevent mitochondrial oxidative damage, and has a hundred of times stronger effect than untargeted coenzyme Q10.¹² A significant challenge in utilizing TPP-conjugated antioxidants for therapeutic purposes lies in their potential mitochondrial toxicity.¹³ Consequently, during clinical evaluations of these compounds, precise dosage regulation is imperative to maintain MTA (mitochondria-targeted antioxidant) concentrations below levels that could compromise mitochondrial integrity and functionality. Conventional approaches to developing MTAs involved the conjugation of TPP with antioxidant moieties, including phenolic structures and flavonoid derivatives. However, these traditional agents typically exhibit a stoichiometric 1:1 interaction with ROS, necessitating administration of substantial quantities to achieve therapeutic efficacy.

We synthesized 4’-hydroxy-2-substituted phenyl nitro nitrogen oxide (HPN, Figure 1A) previously, which is an imidazole nitrogen oxygen free radical antioxidant. HPN has the ability to mimic SOD activity and react with OH radicals in cyclic and catalytic manners, blocking Fenton reaction and inhibiting ROS attacks on biomolecules and biofilms, thereby reducing cellular oxidative damage.^14–16 We found that HPN was able to penetrate the blood–brain barrier and exerted excellent protective effects on HH-induced brain damage.^17,18 However, similar to other nitroxyl radicals, HPN has a small molecular weight, high reactivity, and lacks targeting, resulting in a fast clearance rate and short plasma half-life.¹⁹ These factors limit its application in the prevention of HHBI.

Figure 1 The chemistry structure of HPN (A) and TPP-C6-HPN (B).

Nanotechnology has been widely applied in the development of modern medicine and pharmacy. Nanoparticles have significant advantages in achieving targeted drug delivery and sustained release, enhancing drug stability, improving pharmacokinetics, prolonging blood circulation time and reducing the toxic side effects of drugs.²⁰ Due to the excellent biocompatibility, biodegradability, and unique physicochemical properties of poly(D, L-lactide-co-glycolide, PLGA) copolymers, NPs based on PLGA have been used for drug delivery.^21,22 PLGA has been approved by the US Food and Drug Administration (FDA) and the European Medicines Agency (EMA) for medical use, and is one of the most widely used nanoparticle polymers.²³

With the aim of improving protective efficiency of HPN against HH-induced brain damage, we designed and synthesized a new mitochondrial-targeting HPN derivative (TPP-C₆-HPN, Figure 1B) using triphenylphosphine cations as carriers. In addition, we used PLGA as a nanocarrier to encapsulate the TPP-C₆-HPN to form nanoparticles (TPP-C₆-HPN@PLGA-NPs) for improving the stability and circulation time. Furthermore, we studied the protective effect of TPP-C₆-HPN@PLGA-NPs on the HH-induced brain injury in vivo. Finally, we also monitored the toxic effects of TPP-C₆-HPN@PLGA-NPs on mice.

More at link.

Meditation May Slow the Aging Process and More

Your competent? doctor completely failed at creating protocols on this, didn't s/he? What were they waiting for? A bolt of lightning to strike some sense into their heads? Everything in stroke is a complete shitshow! So, the only thing to do is NOT HAVE A STROKE!

My meditation is forest bathing, I can't do the sit down method.

meditation (62 posts to January 2012)

 Meditation May Slow the Aging Process and More

Every few months, meditation research unlocks something new—and 2025 is no different. From genetic markers of aging to white matter brain scans, new studies are mapping how and why mindfulness affects the mind and body. This year's findings offer both confirmation of long-standing wisdom and surprising new angles, especially around breathwork, time-of-day habits, and brain aging.

1. Meditation May Slow the Aging Process

A study published in Biomolecules compared long-term Transcendental Meditation (TM) practitioners with non-meditators and found:

• Reduced expression of aging-related genes (including a protein called SOCS3, which helps regulate inflammation and energy use in the body. When it's overactive, it can accelerate aging by disrupting cellular repair and increasing stress responses.)
• Better cognitive performance in areas that typically decline with age
• Healthier regulation of the stress-response system.

Together, these findings suggest TM can reduce allostatic load (the cumulative stress burden on the body and brain). The study also points to a potential metabolic shift during and after meditation that may benefit long-term health.

2. Is There a Best Time to Meditate? 

A large-scale behavioral study in Behavioral Sciences analyzed meditation app usage from over 4,000 people. The findings?

• People who meditated around the same time every day were more likely to stick with the habit long-term.
• But people with inconsistent timing actually meditated more often on average.

This shows habit formation isn’t one-size-fits-all. Some people benefit from routine. Others are driven by emotion-based cues, like meditating when they feel stressed. Motivation and emotional rewards may play just as important a role as timing.

3. Your Breathing Style May Influence Brain Health

In a recent preprint study, daily mindfulness practice with slow breathing significantly reduced plasma amyloid beta (Aβ), a biomarker linked to Alzheimer’s risk. Surprisingly, meditation with normal breathing caused Aβ levels to increase.

This adds to the growing evidence that breathwork is a powerful lever in meditation. Slow breathing may enhance the neuroprotective effects of mindfulness, particularly for aging brains.

4. Meditation Reshapes the Brain’s Emotional Wiring

A PLoS One study found that Sahaja Yoga Meditation practitioners had:

• Stronger white matter connections between the amygdala, anterior insula, and anterior cingulate cortex
• Enhanced interhemispheric connectivity (especially between emotional regulation centers)

These structural changes suggest that regular meditation may rewire the brain to support emotional resilience and top-down control—traits often reported by long-term meditators.

5. Does More Meditation Always Mean Less Stress? Not Exactly.

A Clinical Psychological Science study found mixed results when exploring how meditation app use correlated with psychological distress:

• The impact of meditation on stress varied depending on how researchers measured both dosage and distress
• This suggests we need more nuanced tools to track how and why meditation works

It also reinforces that meditation isn’t a panacea. Its benefits often depend on intention, consistency, technique, and personal context.

Meditation Isn’t One-Size-Fits-All

Meditation is a powerful longevity tool. But the newest science reminds us: how, when, and why you meditate can shape your results. Whether you're looking for emotional clarity, cognitive resilience, or long-term brain health, the key is finding a style that works for you.

Want help getting started? Check out our latest guide: The Best Meditation Apps for Every Kind of Practice

Association between C-reactive protein-albumin-lymphocyte index and stroke: an NHANES analysis (1999–2010)

So you found an association. WHAT THE FUCK NEEDS TO BE DONE TO PREVENT THE PROBLEMS? That is what good stroke research should be doing. This is useless for stroke recovery or prevention! I'd have the mentors and senior researchers fired for such crapola!

 Association between C-reactive protein-albumin-lymphocyte index and stroke: an NHANES analysis (1999–2010)

Yizhou Chen^1†, Meifang Liu^2,3†, Yi Zhang⁴, Xiaolin Yang¹, Mengqi Yue¹, Xu Chen¹, Haiqiang Wang¹, Zirong Wang¹, Haocheng Yu¹ and Jing Shi^1,2,3*

¹Yunnan University of Traditional Chinese Medicine, Kunming, Yunnan, China

²First Affiliated Hospital of Yunnan University of Traditional Chinese Medicine, Kunming, Yunnan, China

³Yunnan Provincial Hospital of Traditional Chinese Medicine, Kunming, Yunnan, China

⁴Qingdao Central Hospital, University of Health and Rehabilitation Sciences, Qingdao, Shangdong, China

Edited by
Guanghua Zhai, Nanjing Medical University, China

Reviewed by
Aditya Yashwant Sarode, Columbia University, United States
Gestter Willian Lattari Tessarin, University Center in the North of São Paulo (UNORTE), Brazil
Neel Patel, Staten Island University Hospital, United States

*Correspondence
Jing Shi, 2662831291@qq.com

^†These authors have contributed equally to this work

Received 07 January 2025
Accepted 20 March 2025
Published 02 April 2025

Citation
Chen Y, Liu M, Zhang Y, Yang X, Yue M, Chen X, Wang H, Wang Z, Yu H and Shi J (2025) Association between C-reactive protein-albumin-lymphocyte index and stroke: an NHANES analysis (1999–2010). Front. Neurol. 16:1548666. doi: 10.3389/fneur.2025.1548666

Objective: This cross-sectional study is based on the NHANES (1999–2010) database and aims to explore the potential relationship between the CALLY index and stroke in the U.S. population.

Methods: This cross-sectional study utilized data from NHANES (1999–2010), including 17,511 American participants after data cleaning. Laboratory markers related to the CALLY index were obtained through standardized biological sample collection and analysis procedures performed by trained professionals. Stroke status was determined based on self-reported questionnaires. Various statistical methods were employed to examine the association between the CALLY index and stroke, as well as its predictive efficacy for stroke risk, including multivariable logistic regression, subgroup analysis, RCS analysis, and ROC analysis.

Results: Among the 17,511 participants analyzed, our findings revealed a nonlinear L-shaped negative association between the CALLY index and stroke risk. In Model 3, a higher CALLY index was significantly associated with a lower stroke risk (OR: 0.99, 95% CI: 0.98–0.99, p = 0.045). Additionally, participants in the highest quartile (Q4) of the CALLY index had a 25% lower likelihood of stroke compared to those in the lowest quartile (Q1) (OR: 0.75, 95% CI: 0.58–0.97, p = 0.030). Furthermore, ROC analysis demonstrated that the CALLY index had superior predictive performance for stroke risk compared to the SIRI and SII indices.

Conclusion: A reduced CALLY index may be linked to a higher risk of stroke. Furthermore, the CALLY index demonstrates superior predictive performance compared to the SIRI and SII indices. The association between the CALLY index and stroke risk provides valuable insights for future stroke prevention and management strategies.

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