Purpose: We aimed to retrospectively analyze the clinical features, laboratory and imaging results, and predictors of poor prognosis for patients with an initial diagnosis of autoimmune encephalitis (AE) at the Affiliated Hospital of Zunyi Medical University. Methods: Fifty patients with an initial diagnosis of AE who were admitted to our hospital from May 2014 to May 2018 were enrolled retrospectively. Clinical characteristics and experimental test data, including the neutrophil-to-lymphocyte ratio (NLR), were collected from medical records within 24 h of admission. Independent prognostic factors were determined by multivariate logistic regression analysis. A good or poor prognosis for patients was defined based on the modified Rankin Scale (mRS). The correlation between the immunotherapy latency and prognostic mRS score was determined using the Spearman rank correlation test. Results: Univariate analysis indicated that increased NLR (P = 0.001), decreased lymphocyte counts (P = 0.001), low serum albumin (P = 0.017), consciousness disorders (P = 0.001), epileptic seizures (P = 0.007), extrapyramidal symptoms (P = 0.042), abnormal electroencephalogram (EEG) findings (P = 0.001), abnormal brain magnetic resonance imaging (MRI) findings (P = 0.003), and pulmonary infection complications (P = 0.000) were associated with the poor prognosis of AE. Multivariate logistic regression analysis showed that NLR (odds ratio [OR] 2.169, 95% confidence interval [CI] 1.029–4.570; P < 0.05) was an independent risk factor for predicting the poor prognosis of AE. NLR > 4.45 was suggested as the cut-off threshold for predicting the adverse outcomes of AE. In addition, we revealed that there was a positive correlation between immunotherapy latency and mRS score (r_s = 0.535, P < 0.05). Conclusions: NLR may have predictive value for the poor outcomes of AE. Early initiation of immunotherapy is associated with a good prognosis.

According to the criteria established by the International League Against Epilepsy (ILAE), epilepsy is defined as a disorder characterized by at least two unprovoked seizures occurring more than 24 h apart. Its pathogenesis is closely related to various physiological and pathological factors. Advances in high-throughput metagenomic sequencing have increasingly highlighted the role of gut microbiota dysbiosis in epilepsy. Short-chain fatty acids (SCFAs), the major metabolites of the gut microbiota and key regulators of the gut-brain axis, support physiological homeostasis through multiple mechanisms. Recent studies have indicated that SCFAs not only regulate seizures by maintaining intestinal barrier integrity and modulating intestinal immune responses, but also affect the structure and function of the blood-brain barrier (BBB) and regulate neuroinflammation. This review, based on current literatures, explores the relationship between SCFAs and epilepsy, emphasizing how SCFAs affect epilepsy by modulating the intestinal barrier and BBB. In-depth studies on SCFAs may reveal their therapeutic potential and inform the development of gut microbiota-targeted epilepsy treatments.

Cytomegalovirus (CMV) has successfully established a long-lasting latent infection in humans due to its ability to counteract the host antiviral innate immune response. During coevolution with the host, the virus has evolved various evasion techniques to evade the host’s innate immune surveillance. At present, there is still no vaccine available for the prevention and treatment of CMV infection, and the interaction between CMV infection and host antiviral innate immunity is still not well understood. However, ongoing studies will offer new insights into how to treat and prevent CMV infection and its related diseases. Here, we update recent studies on how CMV evades antiviral innate immunity, with a focus on how CMV proteins target and disrupt critical adaptors of antiviral innate immune signaling pathways. This review also discusses some classic intrinsic cellular defences that are crucial to the fight against viral invasion. A comprehensive review of the evasion mechanisms of antiviral innate immunity by CMV will help investigators identify new therapeutic targets and develop vaccines against CMV infection.

Seizures induce the release of excitatory amino acids (EAAs) from the intracellular fluid to the extracellular fluid, and the released EAAs primarily comprise glutamic acid (Glu) and asparaginic acid (Asp). Glu neurotransmission functions via EAA transporters (EAATs) to maintain low concentrations of Glu in the extracellular space and avoid excitotoxicity. EAAT2, the most abundant Glu transporter subtype in the central nervous system (CNS), plays a key role in the regulation of glutamate transmission. Previous studies have shown that SB203580 promotes EAAT2 expression by inhibiting the p38 mitogen-activated protein kinase (MAPK) signaling pathway, but whether SB203580 upregulates EAAT2 expression in epileptic rats is unknown. This study demonstrated that EAAT2 expression was increased in the brain tissue of epileptic rats. Intraperitoneal injection of a specific inhibitor of p38 MAPK, SB203580, reduced the time to the first epileptic seizure and attenuated the seizure severity. In addition, SB203580 treatment increased the EAAT2 expression levels in the brain tissue of epileptic rats. These results suggest that SB203580 could regulate epileptic seizures via EAAT2.

Dysregulation of the cell cycle is one of the fundamental mechanisms underlying tumorigenesis, making cell cycle-related regulators potential antitumor therapeutic targets. Despite significant advances in understanding cell cycle regulatory networks, there is still a lack of a comprehensive and up-to-date synthesis that integrates the latest mechanistic insights with their translational potential in oncology. This review first systematically outlines the pivotal role of the cyclin-cyclin-dependent kinase (CDK)-cyclin-dependent kinase inhibitor (CKI) axis in driving aberrant cell cycle progression in tumors. Then the complex regulatory mechanisms of the tumor cell cycle were explored from various perspectives, including transcriptional control, post-translational modifications, checkpoint mechanisms, crosstalk with cellular processes, and integration with key signaling pathways. Furthermore, we highlight a series of clinically relevant biomarkers tightly linked to cell cycle dysregulation. Focusing on approved therapeutic agents and natural compounds in clinical trials, current treatment approaches that target the cell cycle and related metabolic pathways were also comprehensively assessed, and their prospects in precision oncology were elaborated. Finally, we discuss persistent challenges, including the incomplete understanding of tumor-specific cell cycle networks and the barriers to the clinical translation of targeted therapies. We advocate for future research to leverage multi-omics integration and systems biology approaches to facilitate more precise and effective cell cycle-directed interventions. This work offers a comprehensive framework that connects the fundamental mechanisms of cell cycle dysregulation in tumors with clinical translation, aiming to accelerate biomarker discovery and the development of next-generation precision oncology strategies.

Epilepsy is a common chronic neurological disease that manifests as recurrent seizures. The incidence and prevalence of epilepsy in women are slightly lower than those in men. Polycystic ovary syndrome (PCOS), a reproductive endocrine system disease, is a complication that women with epilepsy are susceptible to, and its total prevalence is 8%–13% in the female population and sometimes as high as 26% in female epilepsy patients. The rate of PCOS increased markedly in female patients who chose valproate (VPA), to 1.95 times higher than that of other drugs. In addition, patients receiving other anti-seizure medications (ASMs), such as lamotrigine (LTG), oxcarbazepine (OXC), and carbamazepine (CBZ), also have reproductive endocrine abnormalities. Some scholars believe that the increase in incidence is related not only to epilepsy itself but also to ASMs. Epileptiform discharges can affect the activity of the pulse generator and then interfere with the reproductive endocrine system by breaking the balance of the hypothalamic–pituitary–ovarian (HPO) axis. ASMs may also cause PCOS-like disorders of the reproductive endocrine system through the HPO axis. Moreover, other factors such as hormone metabolism and related signalling pathways also play a role in it.