Unilateral Occlusion Research Articles

Correlation between nova volume flow rate and TOF signal intensity ratio: value in unilateral internal carotid artery occlusion

Abstract Background and purposes Non-invasive optimal vessel analysis quantitative magnetic resonance angiography (NOVA-QMRA) has emerged as a valuable tool to characterize cerebral hemodynamics in intracranial atherosclerotic disease (ICAD). Our aim was to explore the eventual correlation between volume flow rate (VFR) measured via NOVA-QMRA and signal intensity ratio (SIR) of time-of-flight (TOF) MRA in M1- and P2-segments bilaterally in patients with unilateral internal carotid artery (ICA) occlusion. Materials and methods Patients with acute, subacute or chronic unilaterall ICA occlusion receiving NOVA-QMRA between June 2019 and June 2021 were retrospectively included. In bilateral M1- and P2-segments VFR was assessed by means of NOVA-QMRA and a region of interest (ROI) was selected to measure TOF SIR. A correlation between TOF SIR and VFR was tested by means of Pearson correlation coefficient. Mean difference of TOF SIR and VFR between ipsilateral (to occluded ICA) and contralateral M1- and P2-segments was analyzed using a two-sided Welch’s t test. Results Fifty-five patients with unilateral ICA occlusion were included (acute: 28; subacute: 8; chronic: 19). Both ipsilateral (r = 0.536, p < 0.001) and contralateral (r = 0.757, p < 0.001) TOF SIR correlated significantly with NOVA VFR. This observation proved especially true for patients with chronic ICA occlusion. Both VFR (165.18 vs 110.60, p < 0.001) and TOF SIR (4.96 vs 2.70, p < 0.001) were higher in contralateral than ipsilateral M1-segments; whereas, the contrary was observed for P2-segments (VFR 72.35 vs 102.12, p < 0.001, TOF SIR 2.87 vs 3.39, p = 0.016). Conclusion The study results showed that TOF SIR significantly correlated with phase-contrast derived flow volume in patients with symptomatic ICA occlusion. This correlation remains the same regardless of the stage of the ischemic stroke (acute vs subacute vs chronic). Furthermore, significantly high VFR and TOF SIR in ipsilateral P2-segments may provide evidence of leptomeningeal collateralization in acute patients. Standardly performed TOF SIR Sequences might be of help for a qualitative evaluation of the flow in M1- and P2-segments in patients with unilateral ICA occlusions. NOVA QMRA allows precise quantitative measurements of the flow in cerebral vessels. Graphical abstract

MiR-126 accelerates renal injury induced by UUO via inhibition PI3K/ IRS-1/ FAK signaling induced M2 polarization and endocytosis in macrophages

To investigate the role and molecular mechanism of miR-126 in unilateral ureteral occlusion (UUO). We used bioinformatics to analyse miRNAs specifically expressed in UUO. The mouse model of UUO was established using RAW264.7 cells cultured in vitro and in vivo. The mice were divided into control group, miR-126-NC (negative control) group and miR-126-KD (knockdown) group. Then the relative expression of miR-126 was detected by quantitative reverse transcription-polymerase chain reaction (qRT-PCR), the renal fibrosis was detected by Masson staining, and the protein expression of CD68, collagen I and collagen III in the kidney was detected by immunofluorescence assay. Immunohistochemistry detects α-SMA expression. Moreover, Western blotting was performed to measure the expressions of p-PI3K, CD163, CD206, CD86, iNOS, IL-1β, p-FAK, p-Rac-1, p-IRS-1 and MMP9. The relative fluorescence intensity of F-actin and p-FAK was detected by immunofluorescence assay, and the phagocytosis ability of macrophages was determined by phagocytosis assay with fluorescent microspheres. Bioinformatics analysis reveals miR-126-specific overexpression in UUO. Successful transfection of miR-126-NC and miR-126-KD was confirmed by RT-PCR. The selective reduction of miR-126 was validated by Masson, immunohistochemistry and immunofluorescence staining to decrease the area of UUO-induced renal fibrosis and to lower the expression of CD68, α-SMA, collagen I, and collagen III. The reduction of iNOS expression may also be achieved with selective knockdown of miR-126, as verified by cell tests. enhances the phagocytic ability of macrophages and the expression of p-PI3K, CD206, p-FAK, F-actin, p-Rac-1, p-IRS-1 and MMP9. MiR-126 can inhibit the PI3K signaling pathway, promote M1 macrophage polarization, and suppress the activation of FAK and Rac-1, thus accelerating the progression of UUO.

Transcriptional responses in a mouse model of silicone wire embolization induced acute retinal artery ischemia and reperfusion.

Acute retinal ischemia and ischemia-reperfusion injury are the primary causes of retinal neural cell death and vision loss in retinal artery occlusion (RAO). The absence of an accurate mouse model for simulating the retinal ischemic process has hindered progress in developing neuroprotective agents for RAO. We developed a unilateral pterygopalatine ophthalmic artery occlusion (UPOAO) mouse model using silicone wire embolization combined with carotid artery ligation. The survival of retinal ganglion cells and visual function were evaluated to determine the duration of ischemia. Immunofluorescence staining, optical coherence tomography, and haematoxylin and eosin staining were utilized to assess changes in major neural cell classes and retinal structure degeneration at two reperfusion durations. Transcriptomics was employed to investigate alterations in the pathological process of UPOAO following ischemia and reperfusion, highlighting transcriptomic differences between UPOAO and other retinal ischemia-reperfusion models. The UPOAO model successfully replicated the acute interruption of retinal blood supply observed in RAO. 60 min of Ischemia led to significant loss of major retinal neural cells and visual function impairment. Notable thinning of the inner retinal layer, especially the ganglion cell layer, was evident post-UPOAO. Temporal transcriptome analysis revealed various pathophysiological processes related to immune cell migration, oxidative stress, and immune inflammation during the non-reperfusion and reperfusion periods. A pronounced increase in microglia within the retina and peripheral leukocytes accessing the retina was observed during reperfusion periods. Comparison of differentially expressed genes (DEGs) between the UPOAO and high intraocular pressure models revealed specific enrichments in lipid and steroid metabolism-related genes in the UPOAO model. The UPOAO model emerges as a novel tool for screening pathogenic genes and promoting further therapeutic research in RAO.

Transcriptional responses in a mouse model of silicone wire embolization induced acute retinal artery ischemia and reperfusion

Acute retinal ischemia and ischemia-reperfusion injury are the primary causes of retinal neural cell death and vision loss in retinal artery occlusion (RAO). The absence of an accurate mouse model for simulating the retinal ischemic process has hindered progress in developing neuroprotective agents for RAO. We developed a unilateral pterygopalatine ophthalmic artery occlusion (UPOAO) mouse model using silicone wire embolization combined with carotid artery ligation. The survival of retinal ganglion cells and visual function were evaluated to determine the duration of ischemia. Immunofluorescence staining, optical coherence tomography, and haematoxylin and eosin staining were utilized to assess changes in major neural cell classes and retinal structure degeneration at two reperfusion durations. Transcriptomics was employed to investigate alterations in the pathological process of UPOAO following ischemia and reperfusion, highlighting transcriptomic differences between UPOAO and other retinal ischemia-reperfusion models. The UPOAO model successfully replicated the acute interruption of retinal blood supply observed in RAO. 60 min of Ischemia led to significant loss of major retinal neural cells and visual function impairment. Notable thinning of the inner retinal layer, especially the ganglion cell layer, was evident post-UPOAO. Temporal transcriptome analysis revealed various pathophysiological processes related to immune cell migration, oxidative stress, and immune inflammation during the non-reperfusion and reperfusion periods. A pronounced increase in microglia within the retina and peripheral leukocytes accessing the retina was observed during reperfusion periods. Comparison of differentially expressed genes (DEGs) between the UPOAO and high intraocular pressure models revealed specific enrichments in lipid and steroid metabolism-related genes in the UPOAO model. The UPOAO model emerges as a novel tool for screening pathogenic genes and promoting further therapeutic research in RAO.

Cerebral perfusion in patients with unilateral internal carotid artery occlusion by dual post-labeling delays arterial spin labeling imaging.

Global and regional cerebral blood flow (CBF) changes in patients with unilateral internal carotid artery occlusion (ICAO) are unclear when the dual post-labeling delays (PLD) arterial spin labeling (ASL) magnetic resonance imaging (MRI) technique is used. Manual delineation of regions of interest for CBF measurement is time-consuming and laborious. To assess global and regional CBF changes in patients with unilateral ICAO with the ASL-MRI perfusion technique. Twenty hospitalized patients with ICAO and sex- and age-matched controls were included in the study. Regional CBF was measured by Dr. Brain's ASL software. The present study evaluated differences in global, middle cerebral artery (MCA) territory, anterior cerebral artery territory, and Alberta Stroke Program Early Computed Tomography Score (ASPECTS) regions (including the caudate nucleus, lentiform nucleus, insula ribbon, internal capsule, and M1-M6) and brain lobes (including frontal, parietal, temporal, and insular lobes) between ICAO patients and controls at PLD 1.5 s and PLD 2.5 s. When comparing CBF between ICAO patients and controls, the global CBF in ICAO patients was lower at both PLD 1.5 s and PLD 2.5 s; the CBF on the occluded side was lower in 15 brain regions at PLD 1.5 s, and it was lower in 9 brain regions at PLD 2.5 s; the CBF in the contralateral hemisphere was lower in the caudate nucleus and internal capsule at PLD 1.5 s and in M6 at PLD 2.5 s. The global CBF in ICAO patients was lower at PLD 1.5 s than at PLD 2.5 s. The ipsilateral CBF at PLD 1.5 s was lower than that at PLD 2.5 s in 15 regions, whereas the contralateral CBF was lower at PLD 1.5 s than at PLD 2.5 s in 12 regions. The ipsilateral CBF was lower than the contralateral CBF in 15 regions at PLD 1.5 s, and in M6 at PLD 2.5 s. Unilateral ICAO results in hypoperfusion in the global and MCA territories, especially in the ASPECTS area. Dual PLD settings prove more suitable for accurate CBF quantification in ICAO.

The Systemic Effect of Ischemia Training and Its Impact on Bone Marrow-Derived Monocytes.

Monocytes are innate immune cells that play a central role in inflammation, an essential component during neovascularization. Our recent publication demonstrated that ischemia training by 24 h unilateral occlusion of the femoral artery (FA) can modify bone marrow-derived monocytes (BM-Mono), allowing them to improve collateral remodeling in a mouse model of hindlimb ischemia. Here, we expand on our previous findings, investigating a potential systemic effect of ischemia training and how this training can impact BM-Mono. BM-Mono from mice exposed to ischemia training (24 h) or Sham (same surgical procedure without femoral artery occlusion-ischemia training) procedures were used as donors in adoptive transfer experiments where recipients were subjected to hindlimb ischemia. Donor cells were divided corresponding to the limb from which they were isolated (left-limb previously subjected to 24 h ischemia and right-contralateral limb). Recipients who received 24 h ischemic-trained monocytes isolated from either limb had remarkable blood flow recovery compared to recipients with Sham monocytes (monocytes isolated from Sham group-no ischemia training). Since these data suggested a systemic effect of ischemic training, circulating extracellular vesicles (EVs) were investigated as potential players. EVs were isolated from both groups, 24 h-trained and Sham, and the former showed increased expression of histone deacetylase 1 (HDAC1), which is known to downregulate 24-dehydrocholesterol reductase (Dhcr24) gene expression. Since we previously revealed that ischemia training downregulates Dhcr24 in BM-Mono, we incubated EVs from 24 h-trained and Sham groups with wild-type (WT) BM-Mono and demonstrated that WT BM-Mono incubated with 24 h-trained EVs had lower gene expression of Dhcr24 and an HDAC1 inhibitor blunted this effect. Next, we repeated the adoptive transfer experiment using Dhcr24 KO mice as donors of BM-Mono for WT mice subjected to hindlimb ischemia. Recipients who received Dhcr24 KO BM-Mono had greater limb perfusion than those who received WT BM-Mono. Further, we focused on the 24 h-trained monocytes (which previously showed downregulation of Dhcr24 gene expression and higher desmosterol) to test the expression of a few genes downstream of the desmosterol pathway, confirm the Dhcr24 protein level and assess its differentiation in M2-like macrophage phenotype. We found that 24 h-trained BM-Mono had greater expression of key genes in the desmosterol pathway, such as liver X receptors (LXRs) and ATP-binding cassette transporter (ABCA1), and we confirmed low protein expression of Dhcr24. Further, we demonstrated that ischemic-trained BM-Mono polarized towards an anti-inflammatory M2 macrophage phenotype. Finally, we demonstrated that 24 h-trained monocytes adhere less to endothelial cells, and the same pattern was shown by WT BM-Mono treated with Dhcr24 inhibitor. Ischemia training leads to a systemic effect that, at least in part, involves circulating EVs and potential epigenetic modification in BM-Mono. These ischemic-trained BM-Mono demonstrated an anti-inflammatory phenotype towards M2 macrophage differentiation and less ability to adhere to endothelial cells, which is associated with the downregulation of Dhcr24 in those cells. These data together suggest that Dhcr24 might be an important target within monocytes to improve the outcomes of hindlimb ischemia.

Injectable Gel-PEG hydrogels as promising delivery system for intravitreal PACAP release: Novel therapeutics for unilateral common carotid artery occlusion induced retinal ischemia

Retinal ischemia is an ophthalmic emergency often caused by cardiovascular diseases, leading to irreversible vision loss and even blindness. Innovative retinal ischemia treatments are needed due to limited options. The pathological mechanisms involve retinal cell apoptosis and microglial activation. The pituitary adenylate cyclase-activating polypeptide (PACAP) is a well distributed neuropeptide found in both central nervous system and peripheral organs. Though it shows great anti-apoptosis and anti-microglia activation properties, it is rapidly cleared by intravitreal injection. Herein, we established a novel poly(ethylene glycol) (PEG) hydrogel system by cross-linking 4arm-PEG-NHS and 4arm-PEG-NH2 to load PACAP (PACAP@Gel-PEG), which exhibited great fluidity, injectability, structural recovery ability, moderate swelling ratio and drug release ability that were appropriate for drug delivery. Then the safety and effectiveness of the PACAP@Gel-PEG were evaluated in vitro in three retinal cell lines (ARPE-19, 661 W and rRMC) and in vivo using the unilateral common carotid artery occlusion (UCCAO) mice model. The CCK-8 test and live/dead staining demonstrated that PACAP@Gel-PEG exhibited excellent biocompatibility in three retinal cell lines. Furthermore, after PACAP@Gel-PEG treatment, a great anti-apoptotic effect was observed in cells treated by CoCl2. Application of PACAP@Gel-PEG greatly improved the therapeutic efficacy of PACAP in restoring retinal function, maintaining retinal integrity, and suppressing apoptosis and microglia activation in retinal tissues. Moreover, in mice, the biosafety of PACAP@Gel-PEG was confirmed by H&E staining of systemic organs. Taken together, our results demonstrated PACAP@Gel-PEG as a promising therapeutic option for retinal ischemia, providing new strategies for vision restoration.

Evaluation of collateral circulation in patients with internal carotid artery occlusion: A clinical and ultrasonographic multicenter study.

Internal carotid artery (ICA) occlusion is the major cause of ischemic stroke. The effect of collateral vessels on cerebral hemodynamics in ICA occlusion remains unclear. This study investigated the correlation between collateral vessels and the peak systolic velocity of the middle cerebral artery (MCA) in patients with ICA occlusion. The relevant collateral vessels included the anterior communicating (ACoA), posterior communicating (PCoA), and internal-external carotid (IECCA) arteries, respectively. Patients with unilateral ICA occlusion (n = 251) underwent transcranial Doppler imaging to detect the peak systolic velocity (PSV) of the MCA and other intracranial arteries. The clinical symptoms were assessed using the National Institutes of Health Stroke Scale (NIHSS). Patients with ACoA collaterals had significantly higher PSVMCA scores and significantly lower NIHSS scores than those without ACoA collaterals (p < 0.001). Patients without any notable collaterals and those with only IECCA had the lowest PSVMCA and highest NIHSS scores. The PSVMCA and NIHSS scores were negatively correlated (r = -0.566, p < 0.001). Collateral circulation patency in unilateral ICA occlusion was closely associated with clinical symptoms, and patients with ACoA collaterals may have favorable outcomes. (ClinicalTrials.gov Identifier: NCT02397655).

Branch retinal artery occlusion in a young patient with Mayer-Rokitansky-Küster-Hauser type 2 syndrome

Abstract: Retinal vascular occlusions are rare in young people, and any occlusion warrants an extensive clinical evaluation to establish the etiology. Cardiac malformations are a source of embolism. We present a case of atrial septal defect (ASD) in a patient with type II Mayer-Rokitansky-Küster-Hauser syndrome, leading to unilateral branch retinal arterial occlusion (BRAO) in a young woman. A 21-year-old woman presented with sudden, painless, blurring of vision, and a superior visual field defect in her right eye. A fundus examination confirmed the BRAO diagnosis. Ocular and systemic evaluation revealed primary amenorrhea, ASD, ectopic kidneys, and pelvic cyst. Any vascular occlusion in a young patient must be thoroughly evaluated, including a detailed systemic history.

Successful use of lithoplasty for re-expansion of covered iliac stents with unilateral occlusion.

Vessel wall calcification is associated with stent under-expansion and in-stent restenosis. The traditional approaches to treat peripheral artery calcification are percutaneous transluminal angioplasty (PTA) and atherectomy. Shockwave intravascular lithotripsy (IVL) uses sonic wave pressure to disrupt calcium of the severely calcified lesions. Published reports of IVL to treat in-stent restenosis are limited to coronary interventions and bare metal platforms. We describe the case of a 55-year-old male with extremely compressed under-expanded covered stents associated with severe wall calcification that resulted in stent occlusion. The IVL system balloon was deployed uneventfully, in a phased manner. Bilateral bare metal stents were also placed in a kissing fashion to further re-expand the arterial segments. Reintervention with IVL facilitated successful revascularization and the stent remained patent at 24 months. Our case highlights the use of IVL as an effective tool in the management of vessel wall calcification both for primary and secondary interventions.

ENDOVASCULAR ANGIOPLASTY FOR REPEATED REVASCULARIZATION OF THE ARTERIAL BED IN PATIENTS WITH RECURRENT CHRONIC ARTERIAL INSUFFICIENCY

Aim. To improve the results of repeated reconstruction of the great vessels in case of relapse of chronic arterial insufficiency by differentiated use of popliteal tibial autovenous bypass grafting and endovascular angioplasty for revascularization of the arteries of the leg. Materials and methods. The long-term results of surgical treatment of 522 patients were examined, including 353 patients with bilateral atherosclerotic occlusion of the aortic-femoral zone and 159 patients with unilateral occlusion of the ileo-femoral segment. At the primary surgical intervention, 98 patients were diagnosed with chronic arterial insufficiency (CAI) of stage II B, in 228 – CAI of stage III, in 196 – chronic critical ischemia of the lower extremities, stage III – IV. In the long-term postoperative period, 146 (27.97 %) late complications were diagnosed, of which 78 (56.1 %) had a relapse of chronic arterial insufficiency. In 36 patients, CAI stage II B was established, and in 42 – CAI stage III. Patients were re-operated in the period of 5.4 ± 1.9 years after primary revascularization. All men were 64.4 ± 3.1 years old. Results. The multilevel atherosclerotic lesions of the reconstructed arterial bed, cicatricial changes after the initial surgical intervention, progressive atherosclerotic lesions of the outflow tract required multi-story shunting operations. The success of shunting surgery depends on sufficient revascularization of the outflow paths – the arterial bed of the ankle segment. Revascularization of the distal arterial bed was achieved using popliteal-tibial autovenous bypass grafting (19 cases) and endovascular angioplasty (30 observations). To reduce peripheral vascular resistance and increase the volume of the peripheral vascular bed in 19 (63.3%) cases, endovascular balloon angioplasty of two tibial arteries was performed simultaneously. The postoperative period in 10 (12.8%) patients was complicated by the development of thrombosis of the reconstruction segment. In 7 cases, thrombosis of the reconstruction segment was eliminated. The using of popliteal-tibial autogenous bypass grafting and endovascular angioplasty during revascularization of the ankle segment provided satisfactory results in repeated reconstructive operations in 87.2 % of cases. Conclusions. For the revascularization of the lower leg arteries, the use of popliteal autovenous shunting and endovascular angioplasty provides 87.2% satisfactory results in repeated reconstructive operations for chronic arterial insufficiency relapse.

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.

Oxygen extraction fraction change in M1-M6 brain regions of patients with unilateral or bilateral middle cerebral artery occlusion.

Cerebral blood flow (CBF) and oxygen extraction fraction (OEF) can be measured using arterial spin labeling (ASL) and quantitative susceptibility mapping (QSM) sequences, respectively. ASL and QSM sequences were performed on 13 healthy participants and 46 patients with unilateral or bilateral Middle cerebral artery (MCA) occlusion. M1-M3 and M4-M6 correspond to anterior, lateral, and posterior MCA territories within the insular ribbon and centrum semiovale, respectively. In patients with unilateral MCA occlusion, significant decreases in CBF were observed in the lesions in M1, M3, M5 and M6 regions, as well as in the contralateral M3 and M5 regions. The OEF of the lesion in the M1-M4 and M6 regions, and the contralateral M1-M3 regions were significantly higher. Additionally, the cerebral metabolic rate of oxygen (CMRO2) in the lesions of the M3 and M6 regions, and the contralateral M3 region, were significantly lower compared to the corresponding regions of healthy participants. For patients with bilateral MCA occlusion, the CMRO2 in the left M5 region and the right M3 and M6 regions were significantly lower than that in the corresponding regions of healthy participants. In conclusion, abnormal hemodynamics occur in the contralateral hemisphere of patients with unilateral MCA occlusion.

Peripapillary Retinal Nerve Fiber Layer Thickness in Patients with Unilateral Retinal Vein Occlusion

Peripapillary Retinal Nerve Fiber Layer Thickness in Patients with Unilateral Retinal Vein Occlusion

Peripapillary Retinal Nerve Fiber Layer Thickness in Patients with Unilateral Retinal Vein Occlusion

Peripapillary Retinal Nerve Fiber Layer Thickness in Patients with Unilateral Retinal Vein Occlusion

Myelin endocytosis by brain endothelial cells causes endothelial iron overload and oligodendroglial iron hunger in hypoperfusion-induced white matter injury.

Hypoperfusion induces significant white matter injury in cerebral vascular disorders, including arteriosclerotic cerebral small vessel disease (aCSVD), which is prevalent among the elderly. Iron transport by blood vessel endothelial cells (BVECs) from the periphery supports oligodendrocyte maturation and white matter repair. This study aims to elucidate the association between iron homeostasis changes and white matter injury severity, and explore the crosstalk between BVECs and oligodendroglial lineage cells. In vivo: C57BL/6 mice were subjected to unilateral common carotid artery occlusion (UCCAO). Invitro: BVECs with myelin pretreatment were co-cultured with oligodendrocyte progenitor cells (OPCs) or organotypic cerebellar slices subjected to oxygen and glucose deprivation. Circulatory iron tends to be stored in aCSVD patients with white matter injury. Myelin debris endocytosis by BVECs impairs iron transport, trapping iron in the blood and away from the brain, worsening oligodendrocyte iron deficiency in hypoperfusion-induced white matter injury. Iron accumulation in BVECs triggers ferroptosis, suppressing iron transport and hindering white matter regeneration. Intranasal holo-transferrin (hTF) administration bypassing the BBB alleviates oligodendrocyte iron deficiency and promotes myelin regeneration in hypoperfusion-induced white matter injury. The iron imbalance between BVECs and oligodendroglial lineage cells is a potential therapeutic target in hypoperfusion-induced white matter injury.

Optimization of an Ischemic Retinopathy Mouse Model and the Consequences of Hypoxia in a Time-Dependent Manner.

The retina is one of the highest metabolically active tissues with a high oxygen consumption, so insufficient blood supply leads to visual impairment. The incidence of related conditions is increasing; however, no effective treatment without side effects is available. Furthermore, the pathomechanism of these diseases is not fully understood. Our aim was to develop an optimal ischemic retinopathy mouse model to investigate the retinal damage in a time-dependent manner. Retinal ischemia was induced by bilateral common carotid artery occlusion (BCCAO) for 10, 13, 15 or 20 min, or by right permanent unilateral common carotid artery occlusion (UCCAO). Optical coherence tomography was used to follow the changes in retinal thickness 3, 7, 14, 21 and 28 days after surgery. The number of ganglion cells was evaluated in the central and peripheral regions on whole-mount retina preparations. Expression of glial fibrillary acidic protein (GFAP) was analyzed with immunohistochemistry and Western blot. Retinal degeneration and ganglion cell loss was observed in multiple groups. Our results suggest that the 20 min BCCAO is a good model to investigate the consequences of ischemia and reperfusion in the retina in a time-dependent manner, while the UCCAO causes more severe damage in a short time, so it can be used for testing new drugs.

Occlusion of vertebral artery and anterior spinal artery in cervical facet dislocation: a prospective study using computed tomography angiography.

A prospective study. To investigate the incidence of vertebral artery (VA) occlusion and whether anterior spinal artery (ASA) is occluded in cervical facet dislocation. University hospital, China. During a 2-year period, 21 conventional patients with cervical facet dislocation were prospectively enrolled. All patients received computed tomography angiography (CTA) to assess the patency of the VA, anterior radiculomedullary arteries (ARAs), and ASA at the time of injury. Clinical data were documented, including demographics, symptomatic vertebrobasilar ischemia, American Spinal Injury Association Impairment Scale (ASIA) grades, and ASA and VA radiological characteristics. VA unilateral occlusion occurred in 5 of 21 patients (24%), including 2 with unilateral facet dislocation and 3 with bilateral facet dislocation. No ASA occlusion was found in all 21 patients, including 5 with VA unilateral occlusion. No patients had symptomatic vertebrobasilar ischemia. VA occlusion occurs in approximately one-fourth of cervical facet dislocations, with infrequent symptomatic vertebrobasilar ischemia. ASA is not occluded following cervical facet dislocation, even with unilateral VA occlusion.

The measurement and correlation analysis of scleral and choroid thickness in branch retinal vein occlusion

To use Optical Coherence Tomography (OCT) to measure scleral thickness (ST) and subfoveal choroid thickness (SFCT) in patients with Branch Retinal Vein Occlusion (BRVO) and to conduct a correlation analysis. A cross-sectional study was conducted. From May 2022 to December 2022, a total of 34 cases (68 eyes) of untreated unilateral Branch Retinal Vein Occlusion (BRVO) patients were recruited at the Affiliated Eye Hospital of Nanchang University. Among these cases, 31 were temporal branch vein occlusions, 2 were nasal branch occlusions, and 1 was a superior branch occlusion. Additionally, 39 cases (39 eyes) of gender- and age-matched control eyes were included in the study. Anterior Segment Optical Coherence Tomography (AS-OCT) was used to measure ST at 6 mm superior, inferior, nasal, and temporal to the limbus, while Enhanced Depth Imaging Optical Coherence Tomography (EDI-OCT) was used to measure SFCT. The differences in ST and SFCT between the affected eye, contralateral eye, and control eye of BRVO patients were compared and analyzed for correlation. The axial lengths of the BRVO-affected eye, contralateral eye, and control group were (22.92 ± 0.30) mm, (22.89 ± 0.32) mm and (22.90 ± 0.28) mm respectively, with no significant difference in axial length between the affected eye and contralateral eye (P > 0.05). The SFCT and ST measurements in different areas showed significant differences between the BRVO-affected eye, contralateral eye in BRVO patients (P < 0.05). The CRT of BRVO-affected eyes was significantly higher than that of the contralateral eyes and the control eyes (P < 0.001). In comparison between BRVO-affected eyes and control eyes, there were no statistically significant differences in age and axial length between the two groups (P > 0.05). However, significant differences were observed in SFCT and temporal, nasal, superior, and inferior ST between the two groups (P < 0.05). The difference in temporal ST between the contralateral eyes and the control eyes was not statistically significant (t = − 0.35, P = 0.73). However, the contralateral group showed statistically significant increases in SFCT, nasal, superior and inferior ST compared to control eyes (t = − 3.153, 3.27, 4.21, 4.79, P = 0.002, 0.002, < 0.001, < 0.001). However, the difference between the CRT of the contralateral and control eyes was not statistically significant (P = 0.421). When comparing SFCT and ST between BRVO-affected eyes with and without macular edema, no statistically significant differences were found (t = − 1.10, 0.45, − 1.30, − 0.30, 1.00; P = 0.28, 0.66, 0.21, 0.77, 0.33). The thickness of SFCT and temporal ST in major BRVO group is higher than the macular BRVO group and the difference was statistically significant (t = 6.39, 7.17, P < 0.001 for all). Pearson correlation analysis revealed that in BRVO patients, there was a significant positive correlation between SFCT/CRT and temporal ST (r = 0.288, 0.355, P = 0.049, 0.04). However, there was no correlation between SFCT/CRT and nasal ST, superior ST, and inferior ST (P > 0.05). In BRVO patients, both SFCT/CRT and ST increase, and there is a significant correlation between SFCT/CRT and the ST at the site of vascular occlusion.

An analysis of clinical characteristics of rare bilateral medial medullary infarction: An observational study.

This study aimed to characterize the risk factors, etiology, clinical manifestations, anatomical characteristics, stroke mechanisms, imaging features, and prognosis of bilateral medial medullary infarction (BMMI). A retrospective analysis was conducted on 11 patients with BMMI who met the inclusion criteria at the Affiliated Hospital of Xuzhou Medical University from January 2013 to January 2023. The patients' imaging and clinical features were analyzed and summarized. Eleven patients (7 male, 4 female), aged 46 to 62 years, met the inclusion criteria. Common clinical presentations included dysarthria (90.9%), dysphagia (90.9%), quadriplegia (81.8%), and so on. Within 72 hours of onset, 8 cases presented with quadriplegia, 2 cases with hemiplegia, and 1 case without limb paralysis. The main risk factor for BMMI was hypertension, followed by diabetes. "Heart appearance" infarcts occurred in 4 cases (36.4%), while "Y appearance" infarcts occurred in 7 cases (63.6%). Among the patients, 3 had unilateral vertebral artery stenosis or occlusion, 5 had bilateral vertebral artery stenosis or occlusion, 2 had normal vertebral basilar artery, and 1 did not undergo cerebrovascular examination. All patients received standardized treatment for cerebral infarction. The prognosis was poor, with 81.8% of patients having an unfavorable outcome, including 1 death, 9 cases of disability, and only 1 patient achieving self-care ability after recovery. BMMI is more prevalent in males aged 45 to 60 years. The main risk factors are hypertension and diabetes. Atherosclerosis is the primary etiological subtype. The main clinical manifestations are dyskinesia, dizziness, quadriplegia, and dysarthria. The prognosis of BMMI is poor. The specific imaging features of "heart appearance" or "Y appearance" infarcts aid in the diagnosis of BMMI.