QTc prolongation after aneurysmal subarachnoid hemorrhage might be associated with worse neurologic outcome in patients receiving microsurgical clipping or embolization of the intracranial aneurysms: a retrospective observational study.

PURPOSE: QT interval prolongation is one of the most common electrocardiographic (ECG) abnormalities in patients with aneurysmal subarachnoid hemorrhage (aSAH). Whether corrected QT interval (QTc) prolongation is associated with perioperative cardiac events and dismal neurological outcome in mid to long-term follow-up in patients after aSAH is insufficiently studied and remains controversial. METHODS: We retrospectively studied the adult (≥ 18 years) patients admitted to our institution between Jan 2018 and Dec 2020 for aSAH who underwent intracranial aneurysm clipping or embolization. The patients were divided into 2 groups (normal and QTc prolongation groups) according to their QTc. To minimize the confounding bias, a propensity score matching (PSM) analysis was performed to compare the neurologic outcomes between patients with normal QTc and QTc prolongation. RESULTS: After screening, 908 patients were finally included. The patients were divided into 2 groups: normal QTc groups (n = 714) and long QTc group (n = 194). Female sex, hypokalemia, posterior circulation aneurysm, and higher Hunt-Hess grade were associated with QTc prolongation. In multiple regression analysis, older age, higher hemoglobin level, posterior circulation aneurysm, and higher Hunt-Hess grade were identified to be associated with worse outcome during 1-year follow-up. Before PSM, patients with QTc prolongation had higher rate of perioperative cardiac arrest or ventricular arrhythmias. After PSM, there was no statistical difference between normal and QTc prolongation groups in perioperative cardiac events. However, patients in the QTc prolongation group still had worse neurologic outcome during 1-year follow-up. CONCLUSIONS: QTc prolongation is associated with worse outcome in patients following SAH, which is independent of perioperative cardiac events.

Brain arteriovenous malformations of the middle cerebral artery region: image characteristics and endovascular treatment based on a new classification system.

BACKGROUND: To date, few studies have investigated the use of endovascular treatment (EVT) for brain arteriovenous malformations (BAVMs) in the supplying area of the middle cerebral artery (MCA). Moreover, no suitable classification was aimed at EVT for MCA-BAVMs. Therefore, this study proposed a new classification. METHODS: This study retrospectively collected 135 MCA­BAVMs. They were classified into four types: Type I BAVMs located above the M1 segment; Type II BAVMs located in the region around the Sylvian fissure; and Type III BAVMs located in the supplying region of the M4 segment and subdivided into types IIIa and IIIb. The relevance of various types of MCA-BAVMs and their imaging characteristics and EVT outcomes was analyzed by ordinary one-way ANOVA, Tukey's multiple comparisons test and the chi-square test. RESULTS: The 135 patients averaged 33.8 ± 14.7 years and included 75 females (55.6%, 75/135). Among them, 15 (11.1%, 15/135), 16 (11.9%, 16/135), 54 (40%, 54/135), and 50 (37%, 50/135) MCA-BAVMs were type I, II, IIIa and IIIb, respectively. After EVT, a good outcome was achieved in 97% of patients. Statistical analysis showed that type I BAVMs were smaller than type II and IIIb BAVMs (P value < 0.05), and type IIIb BAVMs were larger than type I and IIIa BAVMs (P value < 0.05). Deep vein involvement in type I and IIIb BAVMs was more common than in other types (P value < 0.05), and intraventricular hemorrhage (IVH) was also more common (P value < 0.05). The normal morphology in type IIIb was less than that in the other types (P value < 0.05). Type IIIa BAVMs had a higher degree than other types (P value < 0.05). CONCLUSION: The present study demonstrated that the new classification of MCA-BAVMs can be used to evaluate imaging characteristics and EVT outcomes in different types. In addition, EVT may be a safe treatment modality for MCA­BAVMs.

CT angiographic study of the cerebral deep veins around the vein of Galen.

Research on the anatomy of cerebral deep veins (CDVs) around the vein of Galen (VG) is very important and has fundamental clinical significance. Large-scale anatomical studies of CDVs using computed tomography angiography (CTA) are rarely reported. A retrospective study of the CDVs around the VG was conducted in Chinese patients of Han nationality. One hundred cases were included in the final analysis. The patients were aged from 17 to 78 years (mean: 42.3 years). Also, 46% of the patients were female. The diameter of the internal cerebral vein (ICV) at its beginning and termination points ranged from 0.4 to 2.8 mm (1.49 ± 0.39 mm) and 0.4 to 3.5 mm (2.05 ± 0.47 mm), respectively. There was statistical significance regarding the diameter of the ICV at its beginning and termination points (P <0.01). The ICV length ranged from 28.5 to 47.9 mm (36.86 ± 3.74 mm). The length of the straight sinus (SS) ranged from 30.2 to 57.8 mm (43.6 ± 6.37 mm). The length of the VG ranged from 1.5 to 41.8 mm (9.30 ± 4.76 mm). The angle at the VG and SS transition area ranged from 25.4 to 110.6° (77.2 ± 18.0°). This study was a meaningful attempt to conduct anatomical research of CDVs using CTA. Preoperative familiarity with the normal venous structure and its variation around the VG would be helpful for endovascular treatment.

Endovascular treatment of blunt injury of the extracranial internal carotid artery: the prospect and dilemma.

The extracranial internal carotid artery (ICA) refers to the anatomic location that reaches from the common carotid artery proximally to the skull base distally. The extracranial ICA belongs to the C1 segment of the Bouthillier classification and is at considerable risk for injury. Currently, the understanding of endovascular treatment (EVT) for blunt injury of the extracranial ICA is limited, and a comprehensive review is therefore important. In this review, we found that extracranial ICA blunt injury should be identified in patients presenting after blunt trauma, including classical dissection, pseudoaneurysm, and stenosis/occlusion. Computed tomography angiography (CTA) is the first-line method for screening for extracranial ICA blunt injury, although digital subtraction angiography (DSA) remains the "gold standard" in imaging. Antithrombotic treatment is effective for stroke prevention. However, routine EVT in the form of stenting should be reserved for patients with prolonged neurological symptoms from arterial stenosis or considerably enlarged pseudoaneurysm. Endovascular repair is now emerging as a favored therapeutic option given its demonstrated safety and positive clinical and radiographic outcomes.

The prospects and pitfalls in the endovascular treatment of moyamoya disease-associated intracranial aneurysms.

Moyamoya disease (MMD) is characterized by progressive stenosis or occlusion of the distal internal carotid artery and simultaneous formation of collateral vasculature. The fragile alteration and increased hemodynamic stress in the intra- and extracranial vasculature would conjointly result in the formation of intracranial aneurysms in MMD patients. According to our classification, the MMD-associated aneurysms are divided into the major artery aneurysms (MAAs) and non-MAAs. The non-MAAs are further subdivided into the distal choroidal artery aneurysms, moyamoya vessel aneurysms, transdural collateral aneurysms, and anastomosis aneurysms. Currently, endovascular treatment (EVT) has become the main stream for the MMD-associated aneurysms. There is no difference to EVT for the MMD-associated MAAs of the non-stenosed major arteries with that in the non-MMD patients. While it is a big challenge to perform EVT for MMD-associated aneurysms in the stenosed arteries. Generally speaking, the parent arteries of the non-MAAs are slim, and super-selective catheterization is technically difficult. Most of the times, parent artery occlusion with liquid embolic agents or coils can only be performed. The vasculature in MMD patients is fragile; perioperative management and meticulous intraoperative manipulation are also very important to avoid complications during EVT. In spites of the complications, the EVT can bring good outcome in selected cases of MMD-associated aneurysms.

Parent artery occlusion for flow-related aneurysms at the proximal segment of the main feeding arteries of cerebellar arteriovenous malformations.

BACKGROUND: Flow-related aneurysms (FRAs) associated with cerebellar arteriovenous malformations (AVMs) are complicated, and their management is difficult. We performed a retrospective study to explore the efficacy and outcome of parent artery occlusion (PAO) for FRAs at the proximal segment of the main feeding arteries of cerebellar AVMs. MATERIALS AND METHODS: A retrospective study was performed for patients admitted for a cerebellar AVM between January 2015 and December 2019. Patients were included if (a) they presented with a ruptured or symptomatic FRA at the proximal segment of the main feeding arteries of the cerebellar AVM, (b) the cerebellar AVM did not bleed before admission, (c) the FRA was secured via PAO of the parent feeding artery, and (d) the cerebellar AVM was not intentionally managed or embolized through other feeding arteries during hospitalization. RESULTS: Eight patients aged between 27 and 72 (48.6 ± 14.3) years were identified. Eight ruptured and symptomatic FRAs at the proximal segment of the main feeding arteries of the cerebellar AVMs underwent PAO with coils or Onyx while preserving the arteries distal to the aneurysms. All the patients achieved a favorable recovery after treatment in a follow-up ranged from 8 to 48 months. One patient experienced FRA recurrence and underwent a second PAO. CONCLUSIONS: PAO for FRAs at the proximal segment of the main feeding arteries of cerebellar AVMs is a feasible option. This method is effective in preventing re-rupture of the FRAs and relieving the symptoms in the short term, allowing sufficient time for the patients to receive subsequent treatment.

Correction to: Bone mesenchymal stem cell-derived exosomal microRNA-29b-3p prevents hypoxic-ischemic injury in rat brain by activating the PTEN-mediated Akt signaling pathway.

An amendment to this paper has been published and can be accessed via the original article.

Retraction Note: Bone mesenchymal stem cell-derivedexosomal microRNA-29b-3p preventshypoxic-ischemic injury in rat brain byactivating the PTEN-mediated Aktsignaling pathway.

An amendment to this paper has been published and can be accessed via the original article.

Bone mesenchymal stem cell-derived exosomal microRNA-29b-3p prevents hypoxic-ischemic injury in rat brain by activating the PTEN-mediated Akt signaling pathway.

BACKGROUND: Mesenchymal stem cells (MSCs) are suspected to exert neuroprotective effects in brain injury, in part through the secretion of extracellular vesicles like exosomes containing bioactive compounds. We now investigate the mechanism by which bone marrow MSCs (BMSCs)-derived exosomes harboring the small non-coding RNA miR-29b-3p protect against hypoxic-ischemic brain injury in rats. METHODS: We established a rat model of middle cerebral artery occlusion (MCAO) and primary cortical neuron or brain microvascular endothelial cell (BMEC) models of oxygen and glucose deprivation (OGD). Exosomes were isolated from the culture medium of BMSCs. We treated the MCAO rats with BMSC-derived exosomes in vivo, and likewise the OGD-treated neurons and BMECs in vitro. We then measured apoptosis- and angiogenesis-related features using TUNEL and CD31 immunohistochemical staining and in vitro Matrigel angiogenesis assays. RESULTS: The dual luciferase reporter gene assay showed that miR-29b-3p targeted the protein phosphatase and tensin homolog (PTEN). miR-29b-3p was downregulated and PTEN was upregulated in the brain of MCAO rats and in OGD-treated cultured neurons. MCAO rats and OGD-treated neurons showed promoted apoptosis and decreased angiogenesis, but overexpression of miR-29b-3p or silencing of PTEN could reverse these alterations. Furthermore, miR-29b-3p could negatively regulate PTEN and activate the Akt signaling pathway. BMSCs-derived exosomes also exerted protective effects against apoptosis of OGD neurons and cell apoptosis in the brain samples from MCAO rats, where we also observed promotion of angiogenesis. CONCLUSION: BMSC-derived exosomal miR-29b-3p ameliorates ischemic brain injury by promoting angiogenesis and suppressing neuronal apoptosis, a finding which may be of great significance in the treatment of hypoxic-ischemic brain injury.

Endovascular treatment for dural arteriovenous fistulas in the petroclival region.

Petroclival region dural arteriovenous fistulas (DAVFs) are rare and difficult lesions to manage. They often have very complex anatomical structures and can be further divided into the superior petrosal sinus, petrous apex, inferior petrosal sinus, upper clival, and upper clival epidural-osseous DAVFs. Most petroclival region DAVFs should be treated due to their high Cognard grades. Currently, endovascular treatment (EVT) has become the first-line therapeutic option for petroclival region DAVFs. But not all the petroclival region DAVFs could be cured with EVT. When the arterial feeders are large or the DAVF is adjacent to the venous sinus, the success rate may be higher. In petroclival region DAVFs, if EVT can be performed successfully, satisfactory outcome can be anticipated. However, there are some inadvertent complications, which include cranial nerve palsy, subsequent sinus thrombosis, and migration embolization of the internal carotid artery and vertebral artery. Currently, a review of the EVT of petroclival region DAVFs is lacking. In this article, we performed a review of the relevant literature on this issue. In addition, some illustrative cases would be provided to elaborate these specific entities.

Endovascular treatment of the cavernous sinus dural arteriovenous fistula: current status and considerations.

A cavernous sinus dural arteriovenous fistula (CS-DAVF) is an abnormal arteriovenous communication involving the dura mater within or near the CS wall. The dural arteries from the internal carotid artery and external carotid artery supply the CS-DAVF, and the superior ophthalmic vein (SOV) and inferior petrous sinus (IPS) are frequent venous drainers. In CS-DAVF cases, high-risk lesions require treatment. Endovascular treatment (EVT) has been the first-line option for CS-DAVFs. To our knowledge, a review of the EVT of CS-DAVFs is lacking. Therefore, in this paper, we review the available literature on this issue. In addition, some illustrative cases are also provided to more concisely expound the EVT of CS-DAVFs. According to the recent literature, transvenous embolization via the IPS is considered the most effective method for EVT of CS-DAVFs. In addition, the transorbital approach is another reasonable choice. Other venous approaches can also be tried. Because of the low cure rate, transarterial embolization for CS-DAVFs is limited to only highly selected patients. In the EVT of CS-DAVFs, various agents have been used, including coil, Onyx, and n-butyl cyanoacrylate, with coil being the preferred one. In addition, when EVT cannot obliterate the CS-DAVF, stereotactic radiotherapy may be considered. In general, despite various complications, EVT is a feasible and effective method to manage CS-DAVFs by way of various access routes and can yield a good prognosis.

Angiographic study of the transdural collaterals at the anterior cranial fossa in patients with Moyamoya disease.

Unlike its parietal, temporal, and occipital counterparts, the frontal lobe has a broad basal surface directly facing the anterior cranial fossa dura mater which could permit establishment of transdural collaterals (TDCs) with the frontal lobe. Studies on the TDCs from the anterior cranial fossa in moyamoya disease (MMD) are scarce and inadequately investigated. A retrospective study of 100 hemispheres in 50 patients who were diagnosed with MMD by catheter angiography between January 2015 and June 2019 was performed in our institution. TDCs through the anterior ethmoid artery (AEA) or posterior ethmoid artery (PEA) were divided into 3 types respectively based on their respective angioarchitecture. Furthermore, we also studied TDCs to the temporal, parietal, and occipital lobes and collaterals from the posterior circulation to the territory of the anterior cerebral artery. TDCs through the AEA and PEA were identified in 89 (89/100, 89%) and 73 (73/100, 73%) of the hemispheres. The vascularization state of the frontal lobe was good in 89 (89/100, 89%) hemispheres. Rete mirabile and TDCs through the PEA were statistically different among patients with different Suzuki stages. No statistical difference was noted in TDCs through the AEA, frontal TDCs from other sources, and the vascularization state of the frontal lobe with regard to different Suzuki stages. TDCs through the AEA and PEA at the anterior cranial fossa play a very important role in compensating the ischemic frontal lobe. The frontal lobe could be well compensated in most of the patients with TDCs at the anterior cranial fossa.

Targeted endovascular treatment for ruptured brain arteriovenous malformations.

Currently, endovascular treatment (EVT) is recommended for ruptured brain arteriovenous malformation (BAVM). When performing EVT for ruptured BAVM, curative complete embolization without complications is the ideal goal, but, more often than not, it is difficult, impossible, and dangerous. Therefore, EVT targeted toward ruptured focal weak structures plays a very important role. No previous study has comprehensively reviewed the use of targeted EVT for ruptured BAVMs. Therefore, the current paper reviews the available literature on this subject. In BAVM, the ruptured focal weak structures may include flow-related aneurysms, intranidal venous dilated structures, intranidal fistula, and venous varices or ectasia. These ruptured focal weak structures have direct and indirect imaging presentations. The indirect imaging presentations indicate various intracranial hemorrhages. In direct imaging presentations, digital subtraction angiography (DSA) has the highest degree resolution for showing ruptured focal weak structures. In addition, some magnetic resonance (MR) sequences can be useful to identify ruptured focal weak structures. Of all ruptured focal weak structures, flow-related aneurysms are considered the highest risk and require urgent occlusion. Other ruptured weak structures also need to undergo targeted EVT. After targeted EVT, a good prognosis can be obtained. Therefore, the use of targeted EVT for ruptured BAVM is promising.

Dequalinium chloride inhibits the growth of human glioma cells in vitro and vivo: a study on molecular mechanism and potential targeted agents.

BACKGROUND: Our current understanding of the role of dequalinium chloride (DECA) in the progression of glioma remains very limited. This study was aimed to investigate the effect of DECA on human glioma cell lines in vitro and vivo. METHODS: The underlying molecular mechanism was analyzed for developing potential targeted agents. MTT assay, genomic DNA electrophoresis, DAPI staining, TUNEL staining, and wound scratch assay were performed to evaluate the effect of DECA on human glioma cell lines. Bioinformatics methods were used to screen the possible signaling pathway proteins, and the expression of these proteins and the corresponding mRNA was measured. RESULTS: DECA significantly inhibited the growth and proliferation of human glioma cells. Screening of apoptosis-related proteins showed the mRNA expression level of 6 genes was significantly changed after DECA administration. CONCLUSION: This study shows that DECA effectively inhibits the growth of glioma cells in vitro and vivo. DECA may promote glioma cell apoptosis by affecting the expression of NFKB2, HRAS, NF1, CBL, RAF1, and BCL-2 genes.

Downregulation of long noncoding RNA H19 rescues hippocampal neurons from apoptosis and oxidative stress by inhibiting IGF2 methylation in mice with streptozotocin-induced diabetes mellitus.

The diabetes mellitus (DM)-induced reduction of neurogenesis in the hippocampus is consequently accompanied by cognitive decline. The present study set out to define the critical role played by long noncoding RNA H19 (lncRNA H19) in the apoptosis of hippocampal neurons, as well as oxidative stress (OS) in streptozotocin (STZ)-induced DM mice through regulation of insulin-like growth factor 2 (IGF2) methylation. The expression of lncRNA H19 in the hippocampal neurons and surviving neurons were detected. Hippocampal neurons were cultured and transfected with oe-H19, sh-H19, oe-IGF2, or sh-IGF2, followed by detection of the expressions of IGF2 and apoptosis-related genes. Determination of the lipid peroxide and glutathione levels was conducted, while antioxidant enzyme activity was identified. The IGF2 methylation, the binding of lncRNA H19 to DNA methyltransferase, and the binding of lncRNA H19 to IGF2 promoter region were detected. DM mice exhibited high expressions of H19, as well as a decreased hippocampal neurons survival rate. Higher lncRNA H19 expression was found in DM. Upregulated lncRNA H19 significantly increased the expression of Bax and caspase-3 but decreased that of Bcl-2, thus promoting the apoptosis of hippocampal neuron. Besides, upregulation of lncRNA H19 induced OS. LncRNA H19 was observed to bind specifically to the IGF2 gene promoter region and promote IGF2 methylation by enriching DNA methyltransferase, thereby silencing IGF2 expression. Taken together, downregulated lncRNA H19 reduces IGF2 methylation and enhances its expression, thereby suppressing hippocampal neuron apoptosis and OS in STZ-induced (DM) mice.

Spontaneous recession of a posterior cerebral artery aneurysm concurrent with carotid rete mirabile and moyamoya-pattern collateral vessels: a case report.

BACKGROUND: Carotid rete mirabile (RM) is a meshwork of multiple, freely intercommunicating arterioles that reconstitute the absent or hypoplastic segments of the internal carotid artery (ICA). Carotid RM has been reported to be associated with cerebrovascular diseases. However, it is rarely associated with moyamoya-pattern collateral vessels in the posterior cerebral artery (PCA) region and aneurysm. CASE PRESENTATION: A 39-year-old woman was admitted complaining of sudden-onset headache, nausea, and vomiting. Further investigation revealed subarachnoid hemorrhage (SAH), carotid RM, a moyamoya collateral pattern in the PCA region, and a pseudoaneurysm in the moyamoya-like vessels. The patient was treated conservatively, recovered well and was discharged 1 week later. Follow-up angiography showed that the aneurysm had disappeared. CONCLUSIONS: As shown by the present case, we believe that carotid RM could occur in combination with moyamoya-pattern collateral vessels in the PCA region; aneurysms can occur in the moyamoya-like vascular network. Congenital etiology may be the reason for these combinations. Based on our approach in this case, aneurysm located in moyamoya-like vessels can disappear spontaneously after conservative treatment.

Isolated subdural hematoma secondary to Dural arteriovenous fistula: a case report and literature review.

BACKGROUND: Dural arteriovenous fistula (DAVF) is an uncommon subtype among the intracranial arteriovenous malformations, which is characterized by pathological anastomoses between meningeal arteries and dural venous sinuses, meningeal veins, or cortical veins. While intracerebral hemorrhage accounts for most of the hemorrhagic cases in patients with DAVF, isolated subdural hematoma (SDH) is rarely reported. CASE PRESENTATION: A 45-year-old man was admitted for a progressively worsening headache over 2 weeks. Head computed tomography on admission revealed an isodense chronic SDH (CSDH) on the left hemisphere with mild midline shift. Further angiography of the external carotid artery revealed a DAVF at the transverse sinus. The DAVF was embolized via the middle meningeal artery. His CSDH gradually resolved without surgical intervention. In order to further elucidate this rare entity, a review of relevant literature was also conducted. CONCLUSIONS: Isolated SDH is a rare complication of DAVF. In this report, we presented a rare case of CSDH secondary to an intracranial DAVF. According to this case report and our literature review, the so-called benign type of DAVF without cortical venous drainage does not always warrant a benign process and might be complicated with SDH. Careful preoperative investigation is needed for relative young patients presenting with idiopathic or atypical SDH.

Current status of endovascular treatment for dural arteriovenous fistulae in the anterior cranial fossa: A systematic literature review.

Anterior cranial fossa (ACF) dural arteriovenous fistulae (DAVFs) are rare, and a systematic review of the literature is lacking. Such a review is necessary, however, so a systematic PubMed search of related studies was performed. Twenty-four studies were identified, reporting on 48 patients, of whom 39 had definite age and sex information and 33 (84.6%, 33/39) were male. The afflicted patients were between 37 and 80 years old (mean 55.6). Among the 48 patients, 28 (58.3%, 28/48) primarily presented with intracranial hemorrhage, 47 (97.9%, 47/48) had feeding arteries from the anterior ethmoidal artery (AEA) of the ophthalmic artery (OA), and 40 (83.3%, 40/48) had bilateral feeding arteries. All of the cases had high-grade Cognard classifications (III-IV). Among the 48 patients, 43 (89.6%, 43/48) had drainage into the superior sagittal sinus (SSS). In addition, 36 (75%, 36/48) patients were treated via transarterial embolization (TAE). Of these patients, 28 (77.8%, 28/36) were managed via the AEA of the OA. Another 12 (25%, 12/48) patients were treated via transvenous embolization (TVE), 11 of whom (91.7%, 11/12) were treated with the trans-SSS approach. Complete angiographic cure was achieved in 44 (91.7%, 44/48) patients, with 4 (8.3%, 4/48) patients suffering from postprocedural complications. All 48 patients had clear descriptions of follow-up outcomes, with 45 (93.8%, 45/48) patients having a good outcome. Thus, when treating ACF DAVFs, endovascular treatment (EVT) can completely obliterate the fistula point and correct the venous shunting. EVT is therefore an effective treatment for ACF DAVF. Although many complications can occur, this approach achieves good outcomes in most cases.

Clinical importance of the superficial temporal artery in neurovascular diseases: A PRISMA-compliant systematic review.

The superficial temporal artery (STA) plays a very important role in neurovascular diseases and procedures. However, until now, no comprehensive review of the role of STA in neurovascular diseases from a neurosurgical perspective has ever been published. To review research on the clinical importance of STA in neurovascular diseases, a literature search was performed using the PubMed database. Articles were screened for suitability and data relevance. This paper was organized following the Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) guidelines. According to the literature, STA is one of the terminal branches of the external carotid artery and can give off scalp, muscle, and transosseous branches. STA-middle cerebral artery (MCA) bypass is very useful for intracranial ischemic diseases, including moyamoya disease, chronic ICA and MCA insufficiency, and even acute ischemic stroke. For intracranial complex aneurysms, STA bypass remains a major option that can serve as flow replacement bypass during aneurysmal trapping or insurance bypass during temporary parent artery occlusion. Occasionally, the STA can also be involved in dural AVFs (DAVFs) via to its transosseous branches. In addition, the STA can be used as an intraoperative angiography path and the path to provide endovascular treatments. Therefore, STA is a very important artery in neurovascular diseases.

Lentivirus-Mediated Gene Silencing of Lymphocyte Function-Associated Antigen 1 Inhibits Apoptosis of Hippocampal Neurons in Rats with Acute Cerebral Ischemia After Cerebral Lymphatic Blockage.

BACKGROUND/AIMS: Cerebral ischemia is considered to be the most common cause of stroke with high mortality. It occurs as a result of the damage of the hippocampal neurons with lymphocyte function-associated antigen (LFA)-1 being emphasized to play a role in the biological functions of hippocampal neurons. This study was conducted in order to investigate the effects of specific knockdown of LFA-1 expression by lentivirus had on the apoptosis of the hippocampal neurons, simulated by rat models of acute cerebral ischemia after cerebral lymphatic blockage. METHODS: A total of 60 Wistar rats were selected as subjects, among which 50 were used to establish models of the acute cerebral ischemia after cerebral lymphatic blockage, while the remaining 10 rats were treated with the sham operation. The underlying regulatory mechanisms regarding LFA-1 were analyzed with the treatment of si-LFA-1 and LFA-1 vector in the hippocampal CA1 area of brain tissues isolated from the rats with acute cerebral ischemia. The brain water content, electrolyte content, and blood-brain barrier permeability located in ischemic area of rats were measured. TUNEL staining and immunochemistry methods were employed in order to determine the apoptosis rate and positive levels of LFA-1, MMP-9, and Caspase-3. The mRNA and protein levels of related genes were also detected by means of RT-qPCR and western blot assay. RESULTS: The brain water content, Na+ and Ca+ contents, blood-brain barrier permeability, apoptosis rate, positive levels of LFA-1, MMP-9, and Caspase-3 were decreased, and the K+ content was increased in ischemic tissues treated with si-LFA-1. The mRNA and protein levels of LFA-1, MMP-9, Caspase-3, and Bax had all decreased, while the mRNA and protein levels of Bcl-2 were elevated in the hippocampal CA1 area of rat brain tissues treated with si-LFA-1. These situations could be reversed through the up-regulation of LFA-1. CONCLUSION: In conclusion, LFA-1 gene silencing could improve the acute cerebral ischemia after cerebral lymphatic blockage by inhibiting apoptosis of the hippocampal neurons in rats.