Objectives: Previous studies have demonstrated that the paraventricular nucleus of the thalamus (PVT) is a key wakefulness-controlling nucleus in the thalamus. Therefore, PVT may also be involved in the process of general anesthesia. This study intends to explore the role of PVT in isoflurane anesthesia. Methods: In the present study, we used the expression of c-Fos to observe the neuronal activity of PVT neurons under isoflurane anesthesia. We further recorded the effect of isoflurane anesthesia on the calcium signal of PVT glutamatergic neurons in real time with the help of calcium fiber photometry. We finally used chemogenetic technology to specifically regulate PVT glutamatergic neurons, and observed its effect on isoflurane anesthesia and cortical electroencephalography (EEG) in mice. Results: We found that glutamatergic neurons of PVT exhibited high activity during wakefulness and low activity during isoflurane anesthesia. Activation of PVT glutamatergic neuronal caused an acceleration in emergence from isoflurane anesthesia accompanied with a decrease in EEG delta power (1–4 Hz). Whereas suppression of PVT glutamatergic neurons induced a delay recovery of isoflurane anesthesia, without affecting anesthesia induction. Conclusions: Assuming a pharmacokinetic explanation for results can be excluded, these results demonstrate that the PVT is involved in regulating anesthesia emergence.

Background: Soluble programmed cell death 1 (sPD-1) and its ligand (sPD-L1) have emerged as potential biomarkers for early identification and risk stratification in patients with severe pneumonia (SP). However, there is a lack of robust laboratory evidence supporting their clinical utility. This study aimed to explore the relationship between sPD-1/sPD-L1 levels and clinical outcomes in SP patients.Methods: This study included SP patients admitted to the Department of Critical Care Medicine at the Affiliated Hospital of Zunyi Medical University between November 2022 and December 2023. Patients were categorized into survivor and non-survivor groups based on 28-day clinical outcomes. Baseline characteristics and laboratory data were collected upon admission. Serum levels of sPD-1 and sPD-L1 were quantified using enzyme-linked immunosorbent assay. Cox regression analysis was performed to identify prognostic factors, and a nomogram was developed to predict outcomes. The predictive performance of sPD-1, sPD-L1, and their combined indices was evaluated using receiver operating characteristic (ROC) curve analysis.Results: A total of 125 patients with severe pneumonia (SP) were included in this study. Compared to survivors, non-survivors were older, had more severe disease (as indicated by higher SOFA and APACHE II scores), and exhibited lower body mass index (BMI), hemoglobin levels, lymphocyte counts, CALLY index, and albumin levels. Additionally, non-survivors showed significantly elevated levels of systemic inflammatory markers (NLR, PLR, MLR, CLR, CAR, and SII) and higher serum sPD-1 concentrations. Multivariate Cox regression analysis identified age, SOFA score, and sPD-1 levels as independent risk factors for poor prognosis in SP patients. Restricted cubic spline (RCS) curves revealed a linear relationship between age, SOFA score, and the risk of poor prognosis. A nomogram incorporating age, SOFA score, and sPD-1 levels demonstrated strong predictive performance for 28-day mortality in SP patients, with an area under the curve (AUC) of 0.80. Incorporating sPD-1 measurements significantly improves the prognostic accuracy of both SOFA and APACHE II scores in critically ill patients.Conclusion: sPD-1 levels were significantly elevated in non-surviving SP patients, suggesting its potential role as a biomarker for disease severity and immune dysregulation. The combination of sPD-1 with other clinical parameters may provide valuable insights into the prognosis and immune status of SP patients.

Aim. To compare the clinical characteristics of survival and nonsurvival patients with severe acute pancreatitis (SAP) and explore the risk of mortality in SAP patients. Methods. This was a single‐center retrospective study performed in a severe acute pancreatitis diagnosis and treatment center. According to the outcome, SAP patients were divided into survival group and nonsurvival group. One‐way ANOVA or independent t‐test was used to compare the clinical characteristics of two groups of patients. Multivariate retrospective analysis was used to identify risk factors for mortality in SAP patients. Results. A total of 486 SAP patients were included in the study, and the 90‐day mortality for SAP patients was 13.58%. The common etiologies of SAP are biliary tract diseases (69.75%) and hyperlipidemia (17.28%). The most common complications caused by SAP were organ failure (55.14%), ARDS (50.62%), AKI (30.45%), sepsis (27.16%), and abdominal fluid collection (27.57%). There were differences in age, complications, and medical intervention between the nonsurvival group and the survival group. The main causes of death were infection (46.97%), abdominal bleeding (28.79%), and organ failure (9.09%). The binary logistic regression analysis showed that there were significant differences in age, AKI, sepsis, abdominal hemorrhage, organ failure, laparotomy, creatinine, and APTT between the nonsurvival group and the survival group. Conclusion. Age, AKI, sepsis, abdominal hemorrhage, and organ failure are risk factors for mortality in SAP patients. SAP patients with high creatinine and prolonged APTT upon admission require doctors to be vigilant. The main cause of death in SAP patients is pancreatitis‐related organ failure and secondary infection.

The paraventricular thalamus (PVT) is a major component of the midline structure of the thalamus. It is one of the nonspecific nuclei of the thalamus, which plays a great role in the regulation of cortical arousal. PVT, an important node in the central nervous system, sends widespread outputs to many brain regions and also accepts plentiful inputs from many brain regions to modulate diverse functions, including sleep–wake state, attention, memory, and pain. Recently, with the increasing prevalence of sleep disorders and mood disorders, people pay great attention to PVT, which was implicated in arousal and emotional behaviors. Therefore, the main purpose of this review is to illustrate the characteristic of PVT to provide a reference for future research.

Ketamine is a frequently used intravenous anesthetic, which can reversibly induce loss of consciousness (LOC). Previous studies have demonstrated that thalamocortical system is critical for information transmission and integration in the brain. The ventral posteromedial nucleus (VPM) is a critical component of thalamocortical system. Glutamate is an important excitatory neurotransmitter in the brain and may be involved in ketamine-induced LOC. The study used whole-cell patch-clamp to observe the effect of ketamine (30 μM–1000 μM) on glutamatergic neurotransmission in VPM slices. Ketamine significantly decreased the amplitude of glutamatergic spontaneous excitatory postsynaptic currents (sEPSCs), but only higher concentration of ketamine (300 μM and 1000 μM) suppressed the frequency of sEPSCs. Ketamine (100 μM–1000 μM) also decreased the amplitude of glutamatergic miniature excitatory postsynaptic currents (mEPSCs), without altering the frequency. In VPM neurons, ketamine attenuates the glutamatergic neurotransmission mainly through postsynaptic mechanism and action potential may be involved in the process.