Endoscopic endonasal transsphenoidal surgery for unusual sellar lesions: eight cases and review of the literature.

Background: Preoperative imaging for some unusual lesions in the sellar region can pose challenges in establishing a definitive diagnosis, impacting treatment strategies. Methods: This study is a retrospective analysis of eight cases involving unusual sellar region lesions, all treated with endoscopic endonasal transsphenoidal surgery (EETS). We present the clinical, endocrine, and radiological characteristics, along with the outcomes of these cases. Results: Among the eight cases, the lesions were identified as follows: Solitary fibrous tumor (SFT) in one case, Lymphocytic hypophysitis (LYH) in one case, Cavernous sinus hemangiomas (CSH) in one case, Ossifying fibroma (OF) in two cases; Sphenoid sinus mucocele (SSM) in one case, Pituitary abscess (PA) in two cases. All patients underwent successful EETS, and their diagnoses were confirmed through pathological examination. Postoperatively, all patients had uneventful recoveries without occurrences of diabetes insipidus or visual impairment. Conclusion: Our study retrospectively analyzed eight unusual lesions of the sellar region. Some lesions exhibit specific imaging characteristics and clinical details that can aid in preoperative diagnosis and inform treatment strategies for these unusual sellar diseases.

Solitary fibrous tumor in the saddle area treated with neuroendoscopic surgery and proton therapy: A case report and literature review.

Solitary fibrous tumor (SFT) of the central nervous system is a rare fibroblastic tumor of mesenchymal origin. SFTs in the saddle area are much less common. In January 2022, a 43-year-old female patient was admitted with SFT 3 months following partial resection of a microscopic transsphenoidal saddle area tumor at a different hospital. Magnetic resonance imaging indicated that the unresected part of the tumor was significantly enhanced on T1 enhancement, which strongly indicated a recurrence. Subsequently, the patient underwent transnasal endoscopic saddle area tumor resection at our hospital and the tumor was successfully removed. By using postoperative pathology examination, immunohistochemical analysis of Bcl-2, cluster of differentiation 99, STAT6 and vimentin, and a fusion gene test performed by high-throughput sequencing technology, the SFT was definitively diagnosed. Following 3 months of follow-up, the patient was found to have tumor recurrence in the cavernous sinus and absence of tumor growth in the pituitary fossa. Therefore, the patient received proton therapy and tumor growth was controlled effectively.

Gasdermin D serves as a key executioner of pyroptosis in experimental cerebral ischemia and reperfusion model both in vivo and in vitro.

Even though ischemic stroke is among the leading causes of death worldwide, the pathogenic mechanisms underlying ischemia reperfusion (I/R) brain injury remain unclear. Gasdermin D (GSDMD), as an important factor of pyroptotic death execution downstream of caspase-11 (noncanonical inflammasome) and caspase-1 (canonical inflammasome), may be implicated in I/R injury. The current study aimed to investigate the role and possible underlying mechanisms of GSDMD in pyroptosis during I/R injury. Results indicated that the nucleotide-binding oligomerization domain-like receptors (NLR family) pyrin domain containing 3 (NLRP3) inflammasomes were assembled and activated after middle cerebral artery occlusion/reperfusion (MCAO/R), leading to increased levels of IL-1ß and IL-18. Additionally, GSDMD levels were elevated, and its N-terminal fragment (GSDMD-N) was cleaved to induce pyroptosis after MCAO/R, which was partly dependent on caspase-1 activation and its Asp280 amino acid site. Furthermore, it was found that GSDMD-N could bind to membrane lipids and exhibit membrane-disrupting cytotoxicity, depending on its Glu15 and Leu156 amino acid sites. Nevertheless, the C-terminal fragment of gasdermin (GSDMD-C) exhibited an auto-inhibitory effect on GSDMD-N-induced pyroptosis via binding to GSDMD in the cytoplasm. Taken together, this information suggests that GSDMD may participate in caspase-1-mediated pyroptosis during I/R injury both in vivo and in vitro, which could be a potential therapeutic target to reduce brain I/R injury.

Effects of SC99 on cerebral ischemia-perfusion injury in rats: Selective modulation of microglia polarization to M2 phenotype via inhibiting JAK2-STAT3 pathway.

Inhibition of Janus kinases 2-Signal transducers and activators of transcription3 (JAK2-STAT3) pathway has been shown to exert anti-inflammatory actions. SC99, a novel specific inhibitor targeting JAK2-STAT3 pathway, has been verified to negatively modulate platelet activation and aggregation in vitro. In current study, a middle cerebral artery occlusion and reperfusion (MCAO/R) model was established in Sprague Dawley rats and primary cultured microglia was exposed to oxygen and glucose deprivation (OGD/R) in vitro. Different dosages were employed to detect the effects of SC99 on cerebral ischemia-perfusion (I/R) injury and evaluate the underlying mechanisms. Our results showed that intracerebroventricular injection of SC99 (10 mmol/L, 15 µL) produced an effective inhibitory effect on the phosphorylation of JAK2 and STAT3. Correspondingly, SC99 ameliorated neuronal apoptosis and degeneration, neurobehavioral deficits, inflammatory response and brain edema. And SC99 promoted microglia polarization to an anti-inflammatory M2 phenotype. We concluded that SC99 could alleviate brain damage and play an anti-inflammatory action by promoting microglia polarization to an anti-inflammatory phenotype after I/R injury, which provides an emerging and promising alternative to protect the brain against MCAO/R injury in the future investigations.

Loss of Ribosomal RACK1 (Receptor for Activated Protein Kinase C 1) Induced by Phosphorylation at T50 Alleviates Cerebral Ischemia-Reperfusion Injury in Rats.

Background and Purpose- RACK1 (receptor for activated protein kinase C 1) is an integral component of ribosomes with neuroprotective functions. The goal of this study was to determine the role of RACK1 in cerebral ischemia-reperfusion (I/R) injury and the underlying mechanisms. Methods- A middle cerebral artery occlusion/reperfusion model in adult male Sprague Dawley rats (250-280 g) was established, and cultured neurons were exposed to oxygen-glucose deprivation/reoxygenation to mimic I/R injury in vitro. Expression vectors encoding wild-type RACK1 and RACK1 with T50A mutation (T50A) were constructed and administered to rats by intracerebroventricular injection. Results- The potential role of RACK1 in cerebral I/R injury was confirmed by the decreased protein levels of RACK1 within penumbra tissue, especially of neurons. Second, there was an increase in the phosphorylation ratio of RACK1 at the threonine/serine residues at 1.5 hours after middle cerebral artery occlusion onset. Third, based on site-specific mutagenesis, we identified T50 as a key site for RACK1 phosphorylation during I/R. Fourth, wild-type RACK1 overexpression reduced infarct size, neuronal death, neuronal tissue loss, and neurobehavioral dysfunction, while RACK1 (T50A) overexpression exerted opposite effects. Finally, we found that RACK1 phosphorylation at T50 induced a loss of ribosomal RACK1, which switched RACK1 from beclin-1 translation inhibition to autophagy induction following I/R. Conclusions- RACK1 phosphorylation may be a potential intervention target for neurons during I/R; thus, exogenous supplementation of RACK1 may be a novel approach for ameliorating I/R injury.