Effectiveness of vaccination in reducing hospitalization and mortality rates in dialysis patients with Omicron infection in China: A single-center study.

The impact of vaccination on the outcomes of dialysis patients with Omicron infections in China remains unknown. This study aimed to examine the relationship between vaccination and hospitalization as well as all-cause mortality. We included patients who had undergone maintenance hemodialysis (HD) for at least three months at our center. The follow-up period spanned from December 2022 to February 2023. We assessed the connections between vaccination and hospitalization as well as all-cause mortality using univariable and multivariable logistic regression models. Receiver operating characteristic (ROC) curves were used to assess the diagnostic accuracy for hospitalization and all-cause mortality. Ultimately, a total of 427 HD patients with confirmed SARS-CoV-2 infections were included. The patients had a mean age of 54 years, and 59.4% of them were male. Prior to the investigation, 108 patients had received vaccinations, with 81 of them having completed or received booster vaccinations. Throughout the follow-up period, 81 patients were admitted to the hospital, and 39 patients died. Multivariable logistic regression revealed that vaccination significantly decreased all-cause mortality (OR 0.25, 95% CI 0.07-1.94, P = .04). Moreover, completed or booster vaccinations were effective in reducing the hospitalization rate (OR 0.41, 95%CI 0.17-0.99, P = .047). It is noteworthy that both unvaccinated and vaccinated individuals experienced mild symptoms, and the hospitalization rates were relatively low in both groups. Despite the reduced pathogenicity of Omicron compared to previous strains in dialysis patients, both vaccinated and unvaccinated, vaccination still provides benefits for improving the prognosis.

Multiple intracranial enlarging dissecting aneurysms: a case report.

BACKGROUND: Cases of multiple cerebral aneurysms are rare. In this case report, we describe a male patient with multiple, enlarging, and ruptured aneurysms. The two aneurysms were believed to be dissecting aneurysms. CASE DESCRIPTION: A 47-year-old man presented with left limb paralysis. Magnetic resonance imaging revealed a cerebral infarction. Digital subtraction angiography (DSA) identified an aneurysm and occlusion in the right middle cerebral artery (MCA). The MCA aneurysm was remarkably enlarged on the eighth day after cerebral ischemia and was treated using endovascular techniques. Two weeks after the endovascular treatment, the patient experienced a severe headache and became comatose, and a subarachnoid re-hemorrhage was confirmed. The fourth DSA revealed an enlarging dissecting aneurysm in the posterior cerebral artery. The patient died without further treatment. CONCLUSION: Some dissecting aneurysms rapidly enlarge and rupture.

Percutaneous transluminal angioplasty and stenting vs aggressive medical management on stroke or intracranial atherosclerotic stenosis: a systematic review and meta-analysis.

There are currently two main treatment strategies mainly for high-risk patients: percutaneous transluminal angioplasty and stenting (PTAS) and aggressive medical management (AMM). However, the choice between PTAS or AMM remains controversial for patients with stroke or intracranial atherosclerotic stenosis (ICAS). The investigators searched the PubMed, Web of Science, Embase, Scopus, and Cochrane library databases. Randomized controlled trial (RCT) comparing PTAS and AMM for patients with stroke or ICAS were selected. RevMan 5.3 was used to analyze the results and assess risk of bias. The primary endpoints are stroke and death within 30 days after enrollment, or ischemic stroke in the territory of the qualifying artery beyond 30 days, and entire follow-up endpoints. The secondary outcomes were the disabling or fatal stroke, and incidence of death within 3 years. Four studies, 989 patients were included in this article. The AMM group was superior in the entire follow-up endpoint (OR 0.56; 95% CI 0.40, 0.79). The AMM also better in primary endpoint within 30 days (OR 0.32; 95% CI 0.17, 0.61). There was no significant difference beyond 30 days (OR 1.08; 95% CI 0.63, 1.86). The remaining outcomes, such as stroke and death, were not significantly different (P > 0.05). This meta-analysis shows AMM is significantly more effective than PTAS in subjects with ICAS due to the high rate of periprocedural stroke (OR 0.32; 95% CI 0.17, 0.61) and stroke during the entire follow-up (OR 0.56; 95% CI 0.40, 0.79) associated with PTAS. Furthermore, PTAS offers no additional benefits over AMM beyond 30 days (OR 1.08; 95% CI 0.63, 1.86).

Safety of endovascular therapy for symptomatic intracranial artery stenosis: a national prospective registry.

INTRODUCTION: The safety outcomes of endovascular therapy for intracranial artery stenosis in a real-world stetting are largely unknown. The Clinical Registration Trial of Intracranial Stenting for Patients with Symptomatic Intracranial Artery Stenosis (CRTICAS) was a prospective, multicentre, real-world registry designed to assess these outcomes and the impact of centre experience. METHODS: 1140 severe, symptomatic intracranial arterial stenosis (ICAS) patients treated with endovascular therapy were included from 26 centres, further divided into three groups according to the annual centre volume of intracranial angioplasty and stent placement procedures over 2 years: (1) high volume for ≥25 cases/year; (2) moderate volume for 10-25 cases/year and (3) low volume for <10 cases/year. RESULTS: The rate of 30-day stroke, transient ischaemic attack or death was 9.7% (111), with 5.4%, 21.1% and 9.7% in high-volume, moderate-volume and low-volume centres, respectively (p<0.05). Multivariable logistic regression confirmed high-volume centres had a significantly lower primary endpoint compared with moderate-volume centres (OR=0.187, 95% CI: 0.056 to 0.627; p≤0.0001), while moderate-volume and low-volume centres showed no significant difference (p=0.8456). CONCLUSION: Compared with the preceding randomised controlled trials, this real-world, prospective, multicentre registry shows a lower complication rate of endovascular treatment for symptomatic ICAS. Non-uniform utilisation in endovascular technology, institutional experience and patient selection in different volumes of centres may have an impact on overall safety of this treatment.

Long Non-Coding KCNQ1OT1 Promotes Oxygen-Glucose-Deprivation/Reoxygenation-Induced Neurons Injury Through Regulating MIR-153-3p/FOXO3 Axis.

BACKGROUND: Long non-coding RNAs (LncRNAs) have been reported to play important roles in the pathogenesis and development of many diseases, including cerebral ischemia and reperfusion (I/R) injury. In this study, we aimed to investigate the role of LncRNA-Potassium Voltage-Gated Channel Subfamily Q Member 1 opposite strand/antisense transcript 1 (KCNQ1OT1) in cerebral I/R induced neuronal injury, and its underlying mechanisms. METHODS: Primary mouse cerebral cortical neurons treated with oxygen-glucose deprivation and reoxygenation (OGD/R) in vitro and mice subjected to middle cerebral artery occlusion (MCAO) and reperfusion were used to mimic cerebral I/R injury. Small inference RNA (siRNA) was used to knockdown KCNQ1OT1 or microRNA-153-3p (miR-153-3p). Dual-luciferase assay was performed to detect the interaction between KCNQ1OT1 and miR-153-3p and interaction between miR-153-3p and Fork head box O3a (Foxo3). Flow cytometry analysis was performed to detect neuronal apoptosis. qRT-PCR and Western blotting were performed to detect RNA and protein expressions. RESULTS: KCNQ1OT1 and Foxo3 expressions were significantly increased in neurons subjected to I/R injury in vitro and in vivo, and miR-153-3p expression were significantly decreased. Knockdown of KCNQ1OT1 or overexpression of miR-153-3p weakened OGD/R-induced neuronal injury and regulated Foxo3 expressions. Dual-luciferase analysis showed that KCNQ1OT1 directly interacted with miR-153-3p and Foxo3 is a direct target of miR-153-3p. CONCLUSIONS: Our results indicate that LncRNA-KCNQ1OT1 promotes OGD/R-induced neuronal injury at least partially through acting as a competing endogenous RNA (ceRNA) for miR-153-3p to regulate Foxo3a expression, suggesting LncRNA-KCNQ1OT1 as a potential therapeutic target for cerebral I/R injury.

YY1/LncRNA GAS5 complex aggravates cerebral ischemia/reperfusion injury through enhancing neuronal glycolysis.

Yin-Yang 1 (YY1) has been identified as playing critical roles in multiple diseases. However, little is known regarding its roles and mechanisms in cerebral ischemia/reperfusion (I/R) injury. This study is aimed to explore the roles of YY1 in regulating neuronal apoptosis in cerebral I/R injury and its underlying mechanisms. Primary mouse cerebral cortical neurons were isolated and subjected to OGD/R to mimic cerebral I/R injury in vitro. The roles of YY1 on OGD/R-induced neuronal injury were investigated by performing western blotting, quantitative real-time polymerase chain reaction, TUNEL, RNA-binding protein immunoprecipitation, chromatin immunoprecipitation, chromatin isolation by RNA purification assay, glucose uptake assay, lactate production assay, and extracellular acidification rate assay. YY1-binding long non-coding RNAs (LncRNAs) in neurons subjected to OGD/R were identified by RIP and RNA sequencing. The roles of YY1 on cerebral I/R in vivo were detected by assessing neuronbehaviour, infarct size, and neuronal apoptosis. We found that YY1 expression is downregulated, and LncRNA GAS5 is upregulated in neurons subjected to OGD/R. OGD/R treatment promotes YY1 interacting with GAS5 in neurons, and YY1 negatively regulates GAS5 expression by binding to GAS5 promoter to repress its transcription. Besides, YY1 and GAS5 bind to the same region of PFKFB3 promoter to promote PFKFB3 expression and strengthen neuronal glycolysis, resulting in aggravating OGD/R-induced neuronal apoptosis. Knockdown of YY1 or GAS5 protects against I/R-induced ischemic brain damage and improves overall neurological functions in vivo. Overall, YY1 interacts with LncRNA GAS5 to promote PFKFB3 transcription to enhance neuronal glycolysis, resulting in aggravating cerebral I/R injury.

Yin Yang 1 Dynamically Regulates Antiviral Innate Immune Responses During Viral Infection.

BACKGROUND/AIMS: Type I interferon (IFN-1) production and IFN-1 signaling play critical roles in the host antiviral innate immune responses. Although transcription factor Yin Yang 1 (YY1) has been reported to have a dual activator/repressor role during the regulation of interferon beta (IFN-ß) promoter activity, the roles of YY1 in the regulation of upstream signaling pathways leading to IFN-1 induction and IFN-1 signaling during viral infection remain to be elucidated. METHODS: The roles of YY1 in IFN-1 production and IFN-1 signaling were investigated using immunoblotting, real-time PCR, small interfering RNA (siRNA)-mediated YY1 knockdown, YY1 overexpression by transient transfection, and co-immunoprecipitation, using mouse cells. RESULTS: YY1 was shown to interact with STAT1 in the absence of viral infection. Following viral infection, YY1 protein expression levels were decreased. YY1 knockdown led to a considerable downregulation of phosphorylated (p) TBK1 and pIRF3 expressions, while YY1 overexpression significantly upregulated pTBK1 and pIRF3 expression levels and promoted virus-induced IFN-ß production. Additionally, YY1 knockdown led to a significant upregulation of pSTAT1, pSTAT2 and antiviral interferon-stimulated genes, and inhibited viral replication. CONCLUSION: We demonstrated here that YY1 interacts with STAT1 and dynamically regulates the induction of IFN-1 production and activation of IFN-1 signaling in different stages during viral infection.

Curcumin mitigates cerebral vasospasm and early brain injury following subarachnoid hemorrhage via inhibiting cerebral inflammation.

BACKGROUND AND PURPOSE: Subarachnoid hemorrhage (SAH)-induced cerebral vasospasm and early brain injury is a fatal clinical syndrome. Cerebral vasospasm and early brain injury are associated with inflammatory response and oxidative stress. Whether curcumin, which plays important roles to regulate inflammatory cytokines and inhibit oxidative stress, inhibits SAH-induced inflammation and oxidative stress are largely unknown. METHODS: Adult male rats underwent autologous blood injection into prechiasmatic cistern to induce SAH. Curcumin (150 mg/kg) was administered at 0.5, 24 and 48 hr post-SAH. Mortality calculation and neurological outcomes as well as morphological vasospasm of anterior cerebral artery were studied. Superoxide dismutase, lipid peroxidation, and inflammatory cytokines (MCP-1 and TNF-α) expression in prefrontal region were quantified. Furthermore, p65 and phosphor-p65 were quantitatively analyzed. RESULTS: Curcumin remarkedly reduced mortality and ameliorated neurological deficits after SAH induction (p < .05); morphological results showed that cerebral vasospasm in curcumin-treated group was mitigated (p < .05). SAH-induced MCP-1 and TNF-α overexpression were inhibited in curcumin-treated group (p < .05). Importantly, phosphor-p65 was significantly inhibited after curcumin treatment (p < .05). CONCLUSIONS: Curcumin can inhibit SAH-induced inflammatory response via restricting NF-κB activation to alleviate cerebral vasospasm and early brain injury.

Dormant micro arteriovenous malformations lead to recurrent cerebral haemorrhage.

INTRODUCTION: Some micro arteriovenous malformations (AVMs) located in deep brain are undetectable. How to choose a proper timing to detect these AVMs remains unclear. CASE DESCRIPTION: A 21-year-old male patient was admitted to our center for intraventricular haematoma. Digital subtraction angiographies (DSAs) were performed one week and one month respectively after his haemorrhage, but no positive results were obtained. The patient was hospitalized for re-haemorrhage six years later. A micro AVM with two diffused niduses was detected and embolised three months after his re-haemorrhage. The patient recovered without any neurological deficit. DISCUSSION AND EVALUATION: Compressive effects of haematoma and spontaneous obliteration of AVMs might play pivotal roles in negative DSA results. CONCLUSIONS: Strategic and timely use of DSA could identify some dormant re-haemorrhagic AVMs.

Intracranial stents past, present and the future trend: stents made with nano-particle or nanocomposite biomaterials.

Stroke or cerebral vascular accidents are among the leading causes of death in the world. With the availability of Digital Subtraction Angiography, transluminal angioplasty has become feasible in many situations and the role of intracranial stents is becoming ever more important in the management of cerebral vascular diseases. In current review, we outline the chronological development of various stents namely; balloon expandable stent, self-expandable open cell stent, self-expandable close cell stent and the flow diverting stent. Further we discuss their advantages and limitations in terms of stent migration, thromboemboli, damage to vessels during procedure, in-stent stenosis and hyper-perfusion damage. We also discuss the importance of in-situ endothelialization, controlled expandability and hemodynamic manipulation in stent design. Further, we summarized the role and need for further development in the areas of bio-compatible materials, endothelial progenitor cell capture technique, bio-functionalized-magnetic-nano-particles and nanotechnology which are significant in intracranial stent development.

Postoperative hemorrhage in an elderly patient with a glioblastoma multiform and a calcified chronic subdural hematoma.

BACKGROUND: Cases with brain tumor and subdural hematoma are rare; surgical management of the elderly patients with a glioblastoma multiform (GBM) and a chronic subdural hematoma (CSDH) can be intractable. CASE DESCRIPTION: We report a 77-year-old patient, who had a left front lobe GBM and a giant, calcified, left frontoparietaloccipitotemporal CSDH. The patient recovered well from anesthesia after removal of the GBM and CSDH. However, the patient developed severe hemiplegia and aphasia because of the in-situ hemorrhage 1 day later. Laboratory tests indicated disseminated intravascular coagulation (DIC) leading to the postoperative hemorrhage. The patient was left with hemiparesis and alalia after the in-situ hematoma evacuation. CONCLUSIONS: We presume elderly patients have a higher incidence of postoperative hemorrhage in residual intracranial cavity owing to higher possibility to get DIC. A less aggressive surgical management could be a more appropriate choice.