Artery Occlusion Research Articles

Symptoms similar to Kleine–Levin syndrome in a patient with basilar artery occlusion: a case report and literature review

Symptoms similar to Kleine–Levin syndrome in a patient with basilar artery occlusion: a case report and literature review

Hybrid Surgery for symptomatic chronic internal carotid artery occlusion: a single-center experience.

Patients with symptomatic chronic internal carotid artery occlusion (ICAO) face a high risk of recurrent stroke despite receiving aggressive medical therapy. This study aimed to evaluate the effectiveness and safety of hybrid surgery in treating symptomatic chronic ICAO. This retrospective case series was conducted at a single center. From January 2019 to December 2022, patients with symptomatic chronic ICAO who underwent hybrid surgery were included. We collected baseline data, lesion characteristics, revascularization rates, perioperative complications, and follow-up outcomes. The study enrolled 27 patients, comprising 22 males and 5 females, with symptomatic chronic ICAO. The hybrid surgery achieved a technical success rate of 100% for revascularization (n = 27), with a perioperative complication rate of 14.8% (n = 4). Following a median follow-up of 6.0months (IQR, 4-10), 21 patients underwent a DSA or CT angiography reexamination, confirming a vascular patency rate of 90.5% (n = 19). One patient required surgery for severe in-stent restenosis, and another experienced asymptomatic occlusion. Clinical follow-ups were conducted for all 26 patients; no new strokes were reported in the qualifying artery territory, with 13 patients scoring 0, 12 scoring 1, and 1 scoring 2 on the mRS. Although hybrid surgery represent a promising option for treating chronic ICAO, they are also associated with a relatively high incidence of treatment-related complications. The application of composite surgery should be based on standardized technical guidelines and the careful selection of patients who are genuinely at high risk for recurrent strokes.

Popliteal Access for Iliofemoral Occlusive Disease in the Office-Based Catheter Laboratory

ObjectivePopliteal access (PA) as an alternative to conventional femoral access has not been reported in the office-based catheter laboratory setting (OBL) and may be perceived to have higher risks. The purpose of this study is to evaluate the safety and efficacy of popliteal access for endovascular treatment of iliofemoral arterial occlusive disease in an OBL setting. MethodsFrom 10/2018 - 10/2023 a total of 1,408 PAD interventions were performed in our OBL. A cohort of 27 popliteal access consecutive procedures for femoral and iliac artery occlusions were studied. All interventions were done using a micro-puncture needle under ultrasound guidance. All patients were discharged 1 hour after completion of the procedure. Indications for popliteal access were presence of aortoiliac stent/grafts, aorto-bifemoral or aortoiliac bypasses, difficult contralateral or antegrade femoral access, and flush superficial femoral artery (SFA) occlusions. Procedures were determined to be successful upon complete resolution of the target lesions and safety was measured peri-operatively and at 90-days. Patency was determined clinically, by arterial duplex, and by need for reintervention up to 2 years. Results27 popliteal access procedures were performed in 25 patients (21 complete femoral artery occlusions, 6 severe stenosis). Iliac disease was present in 9. Indications for PA were existing aortoiliac stent graft 11, aorto-bifem-iliac bypass 4, non-crossable iliac occlusions 3, failed antegrade femoral access 4, flush SFA occlusion 3, and bilateral common femoral artery disease precluding access 2. TASC pre-op was B: 4, C: 4, D:19. Treatments included atherectomy/balloon angioplasty (BA) and stent 12, BA and stenting 4, atherectomy/BA 5, BA alone 6. Successful opening of occlusions occurred in 25/27 (92.5%). No complications or major adverse cardiac events (MACE) occurred except 1 asymptomatic small popliteal AV fistula. Of the 25 successful procedures duplex patency at 3, 6 & 12 months was 19/20 (95%), 11/15 (69.3%) & 11/13 (61%). Rutherford Classification improved from pre-op > 4 in 24/27 (89%) to post-op < 2 at 1 month in 23/23 (100%), 3 months in 19/20 (95%), 6 months in 11/15 (69.3%), 12 months in 11/13 (61%). Freedom from re-intervention at 3 months in 19/20 (95%), 6 months in 13/15 (86%), and 12 months in 12/13 (79%). ConclusionsPopliteal artery access for complex iliofemoral disease is safe and effective and should be considered as a valid alternative option in the OBL setting.

Jun-activated SOCS1 enhances ubiquitination and degradation of CCAAT/enhancer-binding protein β to ameliorate cerebral ischaemia/reperfusion injury.

This study investigates the molecular mechanisms behind ischaemia/reperfusion (I/R) injury in the brain, focusing on neuronal apoptosis. It scrutinizes the role of the Jun proto-oncogene in apoptosis, involvement of SOCS1 in neural precursor cell accumulation in ischaemic regions, and the upregulation of C-EBPβ in the hippocampus following I/R. Key to the study is understanding how Jun controls C-EBPβ degradation via SOCS1, potentially offering new clinical treatment avenues for I/R. Techniques such as mRNA sequencing, KEGG enrichment analysis and protein-protein interaction (PPI) in mouse models have indicated involvement of Jun (AP-1) in I/R-induced cerebral damage. The study employs middle cerebral artery occlusion in different mouse models and oxygen-glucose deprivation/reoxygenation in cortical neurons to examine the impacts of Jun and SOCS1 manipulation on cerebral I/R injury and neuronal damage. The findings reveal that I/R reduces Jun expression in the brain, but its restoration lessens cerebral I/R injury and neuron death. Jun activates SOCS1 transcriptionally, leading to C-EBPβ degradation, thereby diminishing cerebral I/R injury through the SOCS1/C-EBPβ pathway. These insights provide a deeper understanding of post-I/R cerebral injury mechanisms and suggest new therapeutic targets for cerebral I/R injury. KEY POINTS: Jun and SOCS1 are poorly expressed, and C-EBPβ is highly expressed in ischaemia/reperfusion mouse brain tissues. Jun transcriptionally activates SOCS1. SOCS1 promotes the ubiquitination-dependent C-EBPβ protein degradation. Jun blunts oxygen-glucose deprivation/reoxygenation-induced neuron apoptosis and alleviates neuronal injury. This study provides a theoretical basis for the management of post-I/R brain injury.

The choice of a method for restoring coronary blood flow in myocardial infarction with ST segment elevation (literature review)

In the structure of total mortality, cardiovascular diseases are in the first place in the world. The main and most common reason for this is the incidence of myocardial infarction (MI). The basis of the pathogenesis of MI with ST elevation is persistent and complete thrombotic occlusion of the large epicardial branch of the coronary artery, leading to extensive necrosis of the heart muscle with the development of life-threatening complications, including death, the frequency of which is 8–10 %. The prognosis for MI is influenced by the presence of risk factors, complications, hemodynamic status, polymorbidity, as well as tactics for restoring coronary blood flow. To eliminate acute coronary artery occlusion, conservative treatment is used – thrombolytic therapy, surgical – primary percutaneous intervention, thromboextraction, coronary bypass surgery, as well as their combination. Today, there are scattered and isolated studies characterizing the approach to treatment in patients with MI with ST elevation in various diseases and with polymorbid pathology, the relationship with risk factors and laboratory and instrumental data has not been established, among which predictors of rapid response and death in patients with polymorbid pathology for emergency physicians have not been determined. It can be assumed that the chosen optimal patient management tactics in a specific clinical situation, taking into account the above-mentioned factors, will reduce the development of complications and increase the survival rate of patients with MI.

Pro-Inflammatory Signaling Cascade Markers, Oxidative Stress-Inflammatory Signaling Axis, and Chronic Total Occlusion of Tibial Artery in Elderly Patients Suffering from Occlusion of Coronary Arteries

Introduction: Oxidative response is a risk factor in the progression of arterial atherosclerosis. Objective: This research study aimed to examine the effects of oxidative response on atherosclerotic susceptibility as well as the development of arteriosclerosis occlusions of the tibial artery through pro-inflammatory mediator genes in elderly patients with occlusion of coronary arteries. Methods: We determined that oxidative stress biomarkers (Malondialdehyde-modified Low-density Lipoprotein (MDA-LDL), Oxidized Low-density Lipoprotein (Ox-LDL) as well as Heme Oxygenase- 1 (HO-1)] and the expressions of pro-inflammatory mediator genes [Toll-like Receptor 4 (TLR4), Nuclear Factor kappa-B (NF-κB), Myeloid Differentiating factor 88 (MyD88) and Growth Arrest-specific gene 6 (GAS6)] have an impact on the severity of arteriosclerosis occlusions of tibial artery in elderly patients suffering from occlusion of coronary arteries. Results: Levels of MDA-LDL, Ox-LDL, HO-1, TLR4, NF-κB, MyD88, and GAS6 were increased in the occlusion of tibial arteries + two-vessel coronary occlusion group compared to the CON group and occlusion of tibial arteries + one-vessel coronary occlusion group, respectively (p &lt; 0.001); they were also elevated in occlusion of tibial arteries + multiple-vessel coronary occlusion group compared to occlusion of tibial arteries + one-vessel coronary occlusion group and occlusion of tibial arteries + two-vessel coronary occlusion group, respectively (P &lt; 0.001). This has indicated the key roles of oxidative stress and pro-inflammatory mediator genes in arteriosclerosis occlusions of tibial artery in elderly patients with occlusion of coronary arteries. Conclusion: Oxidative response may promote the expressions of inflammatory genes and enhance susceptibility to arteriosclerosis occlusions of the tibial artery in elderly patients with chronic total coronary occlusions.

Evaluating the Management and Outcomes of Acute Extracranial Occlusions of Internal Carotid Arteries with Patent Intracranial Vasculature

Evaluating the Management and Outcomes of Acute Extracranial Occlusions of Internal Carotid Arteries with Patent Intracranial Vasculature

Stroke pattern in giant-cell arteritis mostly involves watershed areas

ContextStroke related to giant cell arteritis (GCA) is rare and is associated with a poor outcome. One of the putative ischemic mechanisms is narrowing of the arterial lumen due to wall infiltration by inflammation and intimal proliferation, leading to reduced distal blood flow. It was hypothesized that GCA-related stroke could predominate in watershed areas (WA). MethodsLiterature review including all cases of GCA-related stroke with brain images. ResultsAmong 75 cases of GCA-related stroke, the anterior and posterior territories were involved in 48 % and 62.6 %, respectively. Up to 88.9 % of cases of anterior stroke probably involved WA. WA lesions in the posterior territories were as follows: uni/bilateral middle cerebellar peduncle (MCP) lesions in 25.5 %, and with less confidence, non-wedge-shaped cerebellar lesions in 46.8 %, or combined lesions in 61.7 %. Stenosis or occlusion of the afferent artery was almost always observed. A few lesions were not easily explained by low flow. DiscussionDespite the limitations of arterial territory allocation especially in the posterior circulation, ischemic lesions mainly occurred in WA. MCP lesions, which were typically WA, were highly characteristic of GCA. Low flow downstream focal stenosis was the main, but not the unique, ischemic mechanism of GCA stroke.

Endovascular vs Medical Management of Acute Basilar Artery Occlusion

In several randomized clinical trials, endovascular thrombectomy led to better functional outcomes than conventional treatment at 90 days poststroke in patients with acute basilar artery occlusion. However, the long-term clinical outcomes of these patients have not been well delineated. To evaluate 1-year clinical outcomes in patients with acute basilar artery occlusion following endovascular thrombectomy vs control. This study is an extension of the ATTENTION trial, a multicenter, randomized clinical trial. Patients were included between February 2021 and January 2022, with 1-year follow-up through April 2023. This multicenter, population-based study was conducted at 36 comprehensive stroke sites. Patients with acute basilar artery occlusion within 12 hours of estimated symptom onset were included. Of the 342 patients randomized in the ATTENTION trial, 330 (96.5%) had 1-year follow-up information available. Endovascular thrombectomy (thrombectomy group) vs best medical treatment (control group). The primary outcome was defined as a score of 0 to 3 on the modified Rankin Scale (mRS) at 1 year. Secondary outcomes were functional independence (mRS score 0-2), excellent outcome (mRS score 0-1), level of disability (distribution of all 7 mRS scores), mortality, and health-related quality of life at 1 year. Among 330 patients who had 1-year follow-up data, 227 (68.8%) were male, and the mean (SD) age was 67.0 (10.7) years. An mRS score 0 to 3 at 1 year was achieved by 99 of 222 patients (44.6%) in the thrombectomy group and 21 of 108 (19.4%) in the control group (adjusted rate ratio, 2.23; 95% CI, 1.51-3.29). Mortality at 1 year compared with 90 days was more frequent in both the thrombectomy group (101 of 222 [45.5%] vs 83 of 226 [36.7%]) and the control group (69 of 108 [63.9%] vs 63 of 114 [55.3%]). Excellent outcome (mRS score 0-1) at 1 year compared with 90 days increased in the thrombectomy group (62 of 222 [27.9%] vs 45 of 226 [19.9%]) but not in the control group (9 of 108 [8.3%] vs 9 of 114 [7.9%]) resulting in a magnified treatment benefit. Among patients with basilar artery occlusion within 12 hours of onset, the benefits of endovascular thrombectomy at 1 year compared with 90 days were sustained for favorable (mRS score 0-3) outcome and enhanced for excellent (mRS score 0-1) outcome.

Repeated Bow hunter's stroke by artery-to-artery embolism from the vertebral artery dissecting aneurysm formed by head rotation: A case report

A 55-year-old woman suffered from diplopia and occipital pain after shoveling snow. She was diagnosed with the right vertebral artery dissecting aneurysm at the level of the axial vertebra and repeatedly had cerebral infarctions in the posterior circulation. She had subluxation of the atlantoaxial vertebra as an underlying disease. Right vertebral angiogram with the head rotated to the left showed the right vertebral artery occlusion and left vertebral angiogram with the head rotated to the right showed stenosis at the C1-C2 level, leading to the diagnosis of Bow hunter's stroke. After wearing a cervical collar and taking 100 ‍mg of aspirin, she had no recurrence of cerebral infarction and later underwent C1-C2 posterior fusion to prevent the recurrence of cerebral infarction. She finished taking aspirin 6 months after the surgery, and there has been no recurrence of cerebral infarction. We report here a case of Bow hunter's stroke, a rare disease, with good clinical outcomes after C1-C2 posterior fusion.

Investigation of preconditioning and the protective effects of nicotinamide against cerebral ischemia-reperfusion injury in rats

This study investigated the antioxidant and neuroprotective effects of nicotinamide combined with ischemic preconditioning against cerebral ischemia reperfusion (CIR) injury. Thirty-five Wistar albino male rats were randomly divided into five groups: sham, preconditioned ischemia/reperfusion (IP+IR), ischemia/reperfusion (IR), preconditioned ischemia/reperfusion + nicotinamide (IP+IR+N), and ischemia/reperfusion + nicotinamide (IR+N). CIR was achieved with bilateral common carotid artery occlusion. IP+IR and IP+IR+N groups 30 min before ischemia; Three cycles of 10 sec ischemia/30 sec reperfusion followed by 20 min IR were applied. The IP+IR+N and IR+N groups received 500 mg/kg nicotinamide intraperitoneally. After 24 h of reperfusion, a neurological evaluation was performed and vertıcal pole test. Biochemically, malondialdehyde (MDA), glutathione (GSH) levels and catalase (CAT) activity were measured in blood and brain tissue samples. Rates of red neurons, sateliosis and spongiosis were determined histopathologically in the prefrontal cortex areas.After CIR, MDA levels increased significantly in serum and brain tissue in the IR group compared to the sham group, while GSH and CAT activity decreased in the brain tissue (p < 0.05). MDA levels in the tissues were found significantly decreased in the IR+N group compared to the IR group (p < 0.05). Administration of nicotinamide together with IP significantly decreased MDA levels in brain tissue and increased GSH and CAT activity (p < 0.05). Compared to the IR group, the morphological and neurological damage in the prefrontal cortex areas decreased in the IP+IR, IP+IR+N, and IR+N groups (p < 0.05). In addition, red neuron, sateliosis and spongiosis rates increased significantly in the IR group compared to the Sham, IP+IR+N, IR+N groups (p < 0.001 for all). In neurological evaluation, while the neurological score increased and the time on the vertical pole decreased significantly in the IR group, preconditioning, and nicotinamide groups reversed (p < 0.05). The study’s results show that nicotinamide administration with ischemic preconditioning alleviates cerebral ischemia/reperfusion injury.

Nervonic acid protects against oligodendrocytes injury following chronic cerebral hypoperfusion in mice

Chronic cerebral hypoperfusion (CCH) has been acknowledged as a potential contributor to cognitive dysfunction and brain injury, causing progressive demyelination of white matter, oligodendrocytes apoptosis and microglia activation. Nervonic acid (NA), a naturally occurring fatty acid with various pharmacological effects, has been found to alleviate neurodegeneration. Nonetheless, evidence is still lacking on whether NA can protect against neurological dysfunction resulting from CCH. To induce CCH in mice, we employed the right unilateral common carotid artery occlusion (rUCCAO) method, followed by oral administration of NA daily for 28 days after the onset of hypoperfusion. We found that NA ameliorated cognitive function, as evidenced by improved performance of NA-treated mice in both novel object recognition test and Morris water maze test. Moreover, NA mitigated demyelination and loss of oligodendrocytes in the corpus callosum and hippocampus of rUCCAO-treated mice, and prevented oligodendrocyte apoptosis. Furthermore, NA protected primary cultured murine oligodendrocytes against oxygen-glucose deprivation (OGD)-induced cell death in a concentration-dependent manner. These findings indicated that NA promotes oligodendrocyte maturation both in vivo and in vitro. Our findings suggest that NA offers protective effects against cerebral hypoperfusion, highlighting its potential as a promising treatment for CCH and related neurological disorders.

Skin Microvascular Dysfunction in Type 2 Diabetes Mellitus Using Laser Speckle Contrast Analysis and Association with Carotid Intima-Media Thickness.

Background: It is established that diabetes mellitus (DM) is characterized by increased cardiovascular risk associated with subclinical atherosclerosis as well as microvascular alterations. Laser speckle contrast analysis (LASCA) is an innovative, non-invasive method for assessing skin microvascular function. Objectives: We sought to assess skin microvascular function in patients with type 2 DM and matched controls. Methods: Consecutive patients with DM and individuals matched for age, sex and BMI were included in the study. Skin microvascular perfusion was assessed, using LASCA, during baseline, a 5 min occlusion period and a 5 min reperfusion period. Carotid intima-media thickness (cIMT) was measured as a surrogate marker of macrocirculation. Results: In total, 18 patients with DM and 22 in the control group were enrolled. No statistically significant differences were observed in baseline flux, peak flux and percentage decrease during arterial occlusion. During reperfusion, individuals with DM exhibited a smaller peak magnitude compared to controls (147.0 ± 64.7% vs. 189.4 ± 46.0%, respectively; p < 0.05). Moreover, cIMT was higher in patients with DM compared to controls (0.68 ± 0.09 mm vs. 0.60 ± 0.08 mm, respectively, p < 0.01) and was negatively correlated with skin microvascular reactivity in the univariate analysis. In the multivariate analysis, glucose and office systolic blood pressure levels remained significant predictors of microvascular reactivity. Conclusions: Our study shows that patients with type 2 DM exhibit impaired skin microvascular function compared to controls. Furthermore, glucose levels and blood pressure play a key role in microvascular dysfunction. However, additional studies are needed to address the clinical significance of early microvascular changes in DM.

ML218 modulates calcium binding protein, oxidative stress, and inflammation during ischemia-reperfusion brain injury in mice

Cerebral ischemia disrupts calcium homeostasis in the brain causing excitotoxicity, oxidative stress, inflammation, and neuronal cell apoptosis. During ischemic conditions, T-type calcium channel channels contribute to increase in intracellular calcium ions in both neurons and glial cells therefore, the current study hypothesizes the antagonism of these channels using ML218, a novel specific T-Type inhibitor in experimental model of cerebral ischemia-reperfusion (CI/R) brain injury. CI/R injury was induced in Swiss Albino mice by occlusion of common carotid arteries followed by reperfusion. Animals were assessed for learning and memory (MWM), motor coordination (Rota rod), neurological function (neurological deficit score), cerebral infarction, edema, and histopathological alterations. Biochemical assessments were made for calcium binding proteins (Calmodulin- CaM, calcium/calmodulin-dependent protein kinase II-CaMKII, S100B), oxidative stress (4-hydroxy 2-nonenal-4-HNE, glutathione-GSH, inflammation (nuclear factor kappa-light-chain-enhancer of activated B-p65-NF-kB, tumor necrosis factor-TNF-α, interleukin-IL-10) inducible nitric oxide synthase (iNOS) levels, and acetylcholinesterase activity (AChE) in brain supernatants. Furthermore, serum levels of NF-kB, iNOS, and S100B were also assessed. CI/R animals showed impairment in learning, memory, motor coordination, and neurological function along with increase in cerebral infarction, edema, and histopathological alterations. Furthermore, increase in brain calcium binding proteins, oxidative stress, inflammation, and AChE activity along with serum NF-kB, iNOS, and S100B levels were recorded in CI/R animals. Administration of ML218 (5 mg/kg and 10 mg/kg; i.p.) was observed to recuperate CI/R induced impairments in behavioral, biochemical, and histopathological analysis. Hence, it may be concluded that ML218 mediates neuroprotection during CI/R via decreasing brain and serum calcium binding proteins, inflammation, iNOS, and oxidative stress markers.

COVID-19 vaccination and ocular adverse events: a self-controlled case series study from the entire South Korean population

This study aimed to assess the risk of ocular adverse events, including retinal artery occlusion (RAO), retinal vein occlusion (RVO), non-infectious uveitis (NIU), non-infectious scleritis (NIS), optic neuritis (ON), ischemic optic neuropathy (ION), and ocular motor cranial nerve palsy (OMCNP), following coronavirus disease 2019 (COVID-19) vaccination. Population-based self-controlled case series METHODS: This study utilized nationwide claims and vaccination data provided by the Korea National Health Insurance Service and Korea Disease Control and Prevention Agency. From the entire South Korean population of 52 million individuals, patients with incident RAO, RVO, anterior NIU, non-anterior NIU, NIS, ON, ION, or OMCNP between January 2021 and March 2022 were included. The post-vaccination risk period was defined as up to 56 days after COVID-19 vaccination. The relative incidence rate ratios (IRRs) for RAO, RVO, anterior NIU, non-anterior NIU, NIS, ON, ION, and OMCNP during the risk periods were measured using conditional Poisson regression. The study included 6,590, 70,120, 137,958, 17,921, 15,492, 2,039, 49,089, and 11,312 cases of incident RAO, RVO, anterior NIU, non-anterior NIU, NIS, ON, ION, and OMCNP, respectively. The IRRs (95% confidence interval) during the early risk period (0-28 days) were 0.95 (0.88-1.01), 0.96 (0.94-0.98), 0.93 (0.91-0.94), 0.93 (0.89-0.96), 0.96 (0.92-1.01), 1.04 (0.92-1.18), 0.98 (0.95-1.00), and 0.91 (0.86-0.96), respectively. In the late risk period (29-56 days), the IRRs were 0.96 (0.89-1.03), 0.93 (0.91-0.96), 0.96 (0.95-0.98), 1.00 (0.95-1.04), 0.96 (0.91-1.01), 1.00 (0.87-1.15), 1.01 (0.98-1.04), and 0.95 (0.90-1.01), respectively. COVID-19 vaccination did not increase the risk of incident RAO, RVO, anterior NIU, non-anterior NIU, NIS, ON, ION, or OMCNP during the post-vaccination period.

Naoxintong capsule accelerates mitophagy in cerebral ischemia-reperfusion injury via TP53/PINK1/PRKN pathway based on network pharmacology analysis and experimental validation

Ethnopharmacological relevanceThe incidence and mortality of cerebrovascular diseases are increasing year by year. Cerebral ischemia-reperfusion injury (CIRI) is common in patients with ischemic stroke. Naoxintong (NXT) is composed of a variety of Chinese medicines and has the ability to treat CIRI. Aim of the studyThe aim of this study is to investigate whether NXT regulates mitophagy in CIRI based on network pharmacology analysis and experimental validation. Materials and methodsOxygen and glucose deprivation/re-oxygenation (OGD/R, 2/22 h) model of PC12 cells and transient middle cerebral artery occlusion (tMCAO, 2/22 h) model of rats were established. Pharmacodynamic indicators include neurological deficit score, 2,3,5-triphenyte-trazoliumchloride (TTC) staining, hematoxylin-eosin (HE) staining and cell viability. Network pharmacology was used to predict pharmacological mechanisms. Pharmacological mechanism indexes include transmission electron microscopy (TEM), drug affinity responsive target stability (DARTS), cellular thermal shift assay (CETSA), immunohistochemistry (IHC), western blot (WB) and immunofluorescence (IF). Kevetrin (an agonists of p53) and pifithrin-α (an inhibitor of p53) used to detect the key role of p53 in mitophagy of NXT. ResultsNXT (1% serum containing NXT and 110 mg/kg) improved the damage of OGD/R PC12 cells and tMCAO rats, and this protective effect was related to the anti-oxidation and ability to promote mitophagy of NXT. NXT and pifithrin-α increased the expression of promoting-mitophagy targets (PINK1, PRKN and LC3B) and inhibited the expression of inhibiting-mitophagy targets (p52) via restraining p53, and finally accelerated mitophagy caused by CIRI. ConclusionThis study demonstrates that NXT promotes mitophagy in CIRI through restraining p53 and promoting PINK1/PRKN in vivo and in vitro.

Lateral Spinal Artery Aneurysm Causing Subarachnoid Hemorrhage: Literature Review and Case Report.

Ruptured aneurysms of the lateral spinal artery (LSA) causing subarachnoid hemorrhage (SAH) are exceptionally rare. Unlike common aneurysms in the circle of Willis, LSA aneurysms present unique diagnostic and therapeutic challenges due to their complex anatomy. We reviewed the literature, examining case reports detailing LSA aneurysm occurrences, diagnoses, treatments, and complications, and our subsequent analysis highlights the clinical presentations, imaging findings, treatment methods, and anatomical features of the LSA. We identified 10 patients from 7 case reports of LSA aneurysm presenting with SAH, and combined with the present case, this comprised a total of 11 patients. An initial CT angiography identified LSA aneurysm in only 2 of 11 patients, while 5 cases were detected in transfemoral cerebral angiography. Seven patients had stenosis or occlusion of nearby arteries. Among the 10 patients treated, 7 underwent microsurgical clipping, and 3 had endovascular treatment; complications included PICA infarction and subdural hematoma. LSA aneurysms, though rare, should be considered in differential diagnoses of posterior fossa SAH. An accurate diagnosis often requires repeated imaging. It is proposed to individualize treatment strategies based on the unique anatomical structure and hemodynamic conditions of each patient, utilizing both endovascular and surgical approaches. Understanding the vascular anatomy and collateral pathways of the LSA is crucial for improving diagnostic accuracy and treatment outcomes.

Magnitude of systolic blood pressure reduction following endovascular treatment and clinical outcomes in acute large artery occlusion stroke

BackgroundThe impact of lowering systolic blood pressure (SBP) following endovascular treatment (EVT) in acute large vessel occlusion stroke (LVOS) patients remains unclear. We aimed to explore the effect of the...

The effects and significance of Dicyclopentadiene on the expression of Intersectin-1 after cerebral ischemia-reperfusion in rats

ObjectiveThis study mainly observed the changes in Intersectin-1 (ITSN-1) expression in rat brain tissue after ischemia-reperfusion intervened by Dicyclopentadiene. MethodsSD rats were randomly divided into non-middle Cerebral Artery Occlusion model group (normal group, sham operation group) and Middle Cerebral Artery Occlusion (MCAO) model group [Ischemia reperfusion (cerebral ischemia reperfusion)] reperfusion,IR) (6h, 24h, 72h, 1w, 2w) group, butylphthalein intervention group], First of all, Use Western The expression of ITSN-1 in the cerebral tissue of infarction side after ischemia-reperfusion injury in each group was measured by blotting, and then the loss and degree of nerve function after ischemia-reperfusion injury in each group was evaluated by Zea-Longa scoring method. The morphological changes of cells in the ischemic penumbra region in the normal group and the MCAO model group for 24h were observed by HE staining. Next, 24h was selected as the reperfusion point for intervention with butylphthalein sodium chloride injection. Finally, Zea-Longa scoring method was used to evaluate whether the rats had neurological impairment and its degree, TTC (Triphenyltetrazolium chloride) staining was used to determine whether the rats had cerebral infarction and its extent, and Western The expression of ITSN-1 in the cerebral tissue of infarcted rats after ischemia-reperfusion injury was measured by blotting. Results1. Zea-Longa scoring: Scores, except for the normal group and sham operation group (which scored 0), ranged between 2.75 ± 0.46 in the ischemia-reperfusion 24h group and 1.88 ± 0.35 in the Dicyclopentadiene intervention group, showing statistically significant decreases (P<0.05). 2. HE staining results: The cell structures in the brain tissues of normal group rats were normal with regular nuclear shapes and sizes. There were no obvious abnormal changes. Rats in the ischemia-reperfusion 24h group showed obviously swollen cells, reduced and aggregated nucleus, and cell necrosis in the ischemic penumbra. 3. TTC staining results: Except for the normal group and the sham operation group, which had no infarcts, the ischemia-reperfusion 24h group had the largest volume ratio of cerebral infarction. The volume ratio of cerebral infarction in the Dicyclopentadiene intervention group relatively reduced, making a difference with statistical significance (P<0.05). 4. Western blotting results: After cerebral ischemia-reperfusion in rats, ITSN-1 expression in the infarction-side brain tissue dynamically changed. ITSN-1 expression in the ischemia-reperfusion 24h group was significantly lower among other groups compared to the normal group (P<0.05). After 24 hours, the expression gradually increased after using Dicyclopentadiene intervention, the difference was statistically significant (P<0.05). ConclusionAfter cerebral ischemia-reperfusion in rats, ITSN-1 expression dynamically changed in the infarction-side brain tissue. Dicyclopentadiene can alleviate ischemia-reperfusion injuries in rats, which might be related to the regulation of ITSN-1 expression.

Clinical outcomes of reperfusion therapy in patients with site-specific basilar artery occlusion

BackgroundDespite its low incidence, basilar artery occlusion (BAO) remains a major therapeutic challenge since severe disability and death occur in about 80% of patients. Specific site of BAO (proximal, middle,...