The Ang-(1-7)/MasR axis ameliorates neuroinflammation in hypothermic traumatic brain injury in mice by modulating phenotypic transformation of microglia.

The Ang-(1-7)/MasR axis is critically involved in treating several diseases; For example, Ang-(1-7) improves inflammatory response and neurological function after traumatic brain injury and inhibits post-inflammatory hypothermia. However, its function in traumatic brain injury (TBI) combined with seawater immersion hypothermia remains unclear. Here, we used a mice model of hypothermic TBI and a BV2 cell model of hypothermic inflammation to investigate whether the Ang-(1-7)/MasR axis is involved in ameliorating hypothermic TBI. Quantitative reverse transcription PCR, western blotting assay, and immunofluorescence assay were performed to confirm microglia polarization and cytokine regulation. Hematoxylin-eosin staining, Nissl staining, and immunohistochemical assay were conducted to assess the extent of hypothermic TBI-induced damage and the ameliorative effect of Ang-(1-7) in mice. An open field experiment and neurological function scoring with two approaches were used to assess the degree of recovery and prognosis in mice. After hypothermic TBI establishment in BV2 cells, the Ang-(1-7)/MasR axis induced phenotypic transformation of microglia from M1 to M2, inhibited IL-6 and IL-1ß release, and upregulated IL-4 and IL-10 levels. After hypothermic TBI development in mice, intraperitoneally administered Ang-(1-7) attenuated histological damage and promoted neurological recovery. These findings suggest that hypothermia exacerbates TBI-induced damage and that the Ang-(1-7)/MasR axis can ameliorate hypothermic TBI and directly affect prognosis.

Adenomyosis Accompanied by Multiple Hemorrhagic Cerebral Infarction: A Case Report.

This study aims to present a case of uterine adenomyosis accompanied by multiple hemorrhagic cerebral infarctions (CIs), summarize therapeutic experiences based on the literature review, and improve the clinical diagnosis and treatment of multiple hemorrhagic CIs. This paper describes a 46-year-old female with a four-year history of uterine adenomyosis complicated by multiple hemorrhagic CIs. During treatment, elevated levels of D-dimer, CA-125, and severe anemia were observed. Following internal medicine treatment targeting uterine adenomyosis and hemorrhagic CIs, the cerebral hemorrhage gradually resolved. Women presenting with multiple CIs, particularly hemorrhagic ones, should be evaluated for the presence of gynecological diseases. Treating gynecological conditions may aid in the management of multiple CIs.

TAK-3 Inhibits Lipopolysaccharide-Induced Neuroinflammation in Traumatic Brain Injury Rats Through the TLR-4/NF-κB Pathway.

Purpose: The activation of the inflammatory response is regarded as a pivotal factor in the pathogenesis of TBI. Central nervous system infection often leads to the exacerbation of neuroinflammation following TBI, primarily caused by Gram-negative bacteria. This study aims to elucidate the effects of the novel anti-inflammatory drug TAK-3 on LPS-induced neuroinflammation in TBI rats. Methods: In conjunction with the rat controlled cortical impact model, we administered local injections of Lipopolysaccharide to the impact site. Subsequently, interventions were implemented through intraperitoneal injections of TAK-3 and NF-κB activitor2 to modulate the TLR4/NF-κB axis The impact of LPS on neurological function was assessed using mNSS, open field test, and brain water content measurement. Inflammatory markers, including TNF-α, IL-1ß, IL-6 and IL-10 were assessed to evaluate the condition of neuritis by Elisa. The activation of the TLR-4/NF-κB signaling pathway was detected by immunofluorescence staining and Western blot to assess the anti-inflammatory effects of TAK-3. Results: The administration of LPS exacerbated neurological damage in rats with TBI, as evidenced by a reduction in motor activity and an increase in anxiety-like behavior. Furthermore, LPS induced disruption of the blood-brain barrier integrity and facilitated the development of brain edema. The activation of microglia and astrocytes by LPS at the cellular and molecular levels has been demonstrated to induce a significant upregulation of neuroinflammatory factors. The injection of TAK-3 attenuated the neuroinflammatory response induced by LPS. Conclusion: The present study highlights the exacerbating effects of LPS on neuroinflammation in TBI through activation of the TLR-4/NF-κB signaling pathway. TAK-3 can modulate the activity of this signaling axis, thereby attenuating neuroinflammation and ultimately reducing brain tissue damage.

Complex torcular dural arteriovenous fistula leading to cortical venous reflux-induced severe varix and subsequent bilateral cerebral hemispheric hemorrhage: a case report.

Background and importance: Dural arteriovenous fistulas (dAVFs) with cortical venous reflux (CVR) are associated with a higher incidence of intracranial hemorrhage (ICH). We report a rare case of a complex torcular dAVF with severe cortical veins (CV) varix leading to extensive bilateral cerebral hemorrhages. This discovery suggests a potential new subtype of dAVF. The case underscores the necessity of a comprehensive understanding of hemodynamic changes in dAVFs and the importance of considering venous compensatory capacity in treatment. This case challenges existing classifications and treatment strategies for dAVFs, highlighting the need for further research and discussion within the neurosurgical community. Clinical presentation: A 56-year-old male was admitted to the hospital presenting with dizziness, fatigue, and numbness. Brain CT scans revealed extensive bilateral cerebral hemorrhages. Digital subtraction angiography (DSA) identified a complex torcular dAVF. No cerebral sinus venous thrombosis was detected, but a venous variation in the left transverse sinus was observed. Preoperative DSA demonstrated the patient's well-developed venous compensatory ability. Subsequently, the patient underwent transarterial embolization. The patient made a good recovery. Follow-up DSA and MR angiography at 3 months and 1 year post-treatment showed no recurrence. Conclusion: DAVFs are rare lesions, prone to ICH, particularly when CVR is involved. We report a rare case of CVR with severe varix leading to hemorrhagic lesions in both cerebral hemispheres. Our aim is to alert neurosurgical colleagues worldwide to this potential new subtype and to evaluate treatment options, in order to assist those who may encounter such cases in the future.