Viral infection and spread are inhibited by the polyubiquitination and downregulation of TRPV2 channel by the interferon-stimulated gene TRIM21.

Interferon (IFN) contributes to the host's antiviral response by inducing IFN-stimulated genes (ISGs). However, their functional targets and the mechanism of action remain elusive. Here, we report that one such ISG, TRIM21, interacts with and degrades the TRPV2 channel in myeloid cells, reducing its expression and providing host protection against viral infections. Moreover, viral infection upregulates TRIM21 in paracrine and autocrine manners, downregulating TRPV2 in neighboring cells to prevent viral spread to uninfected cells. Consistently, the Trim21-/- mice are more susceptible to HSV-1 and VSV infection than the Trim21+/+ littermates, in which viral susceptibility is rescued by inhibition or deletion of TRPV2. Mechanistically, TRIM21 catalyzes the K48-linked ubiquitination of TRPV2 at Lys295. TRPV2K295R is resistant to viral-infection-induced TRIM21-dependent ubiquitination and degradation, promoting viral infection more profoundly than wild-type TRPV2 when reconstituted into Lyz2-Cre;Trpv2fl/fl myeloid cells. These findings characterize targeting the TRIM21-TRPV2 axis as a conducive strategy to control viral spread to bystander cells.

Postoperative epidural hematoma as a rare complication after intracranial tumor resection: a case series report and causes analysis.

BACKGROUND: To review the treatment and the causes of postoperative epidural hematoma (PEDH) after intracranial tumor resection. METHOD: A retrospective case study was conducted to examine a series of patients who developed PEDH as a complication following intracranial tumor resection between January 2016 and June 2021. The study collected data from hospital charts, including clinical status at admission, imaging results, histopathologic findings, surgical management, complications, and outcomes. Causes of PEDH were evaluated through a review of operative notes and discussions with the surgical team. RESULTS: Twenty-five patients (10 males, 15 females; median age 42 years, range 11-61 years; median medical history 27 months, range 1-96 months) were enrolled in the study. Regarding tumor location, 16 cases exhibited supratentorial brain tumors, 4 cases had infratentorial brain tumors, 2 cases of tumors occurred in the petroclival region, 2 cases in the peritorcular region, and 1 case in the pineal region. Four of these cases were complicated with supratentorial hydrocephalus. The 25 cases in this study were classified into four types based on location. Type 1 refers to EDHs that occur at the adjacent site of the operative field without involvement of the surgical area. Type 2 includes hematomas that occur at the adjacent site of the surgical area and the surgical area. Type 3 includes EDHs that occur in distant areas, and type 4 involves EDHs in the surgical field. The numbers of cases of types 1, 2, 3, and 4 PEDHs were 16, 2, 3, and 4 cases, respectively. Most PEDHs were associated with reduced ICP after craniotomy due to intracranial tumor resection and substantial loss of CSF. All patients achieved satisfactory outcomes after hematoma evacuation. CONCLUSION: The decrease in ICP resulting from intracranial tumor resection and CSF loss might lead to PEDHs. By employing optimized surgical techniques and meticulous patient management to prevent rapid decreases in ICP and dural detachment, we can potentially lower the incidence of PEDHs. Additionally, prompt evacuation of hematomas can contribute to positive outcomes.

Association of HbA1c with carotid artery plaques in patients with coronary heart disease: a retrospective clinical study.

BACKGROUND AND AIMS: Haemoglobin A1c (HbA1c) levels have been shown to be related to carotid artery plaques. However, studies on the relationship between HbA1c levels and carotid artery plaques in patients with coronary heart disease (CHD) are limited and inconsistent. Our objective was to examine the correlation between HbA1c levels and carotid artery plaques in patients with CHD. METHODS: The study comprised 9275 Chinese adults with CHD from January 1, 2014, to September 30, 2020. HbA1c levels were assessed, and colour Doppler ultrasound was used to evaluate the carotid artery, including plaque presence, intima-media thickness, and plaque echo properties, to investigate the association between HbA1c and carotid plaque. A logistic regression model was used to assess the association between carotid artery plaques, carotid plaque echogenicity, and HbA1c. RESULTS: The HbA1c level of the plaque-present group was higher than that of the plaque-absent group [6.1 (5.6-7.2) vs. 5.8 (5.5-6.5), p < 0.001]. In multiple linear regression analysis, intima-media thickness was associated with HbA1c (p < 0.001). Logistic regression showed that a higher HbA1c level was associated with plaque incidence as well as hyperechoic and heterogeneous plaques (p < 0.001). These associations persist after adjusting for age, sex, blood pressure, lipid profiles, alcohol consumption, and tobacco exposure. CONCLUSION: HbA1c levels are notably associated with carotid artery plaque incidence, intima-media thickness, and plaque echogenicity in patients with CHD. These findings show that different levels of HbA1c may be an indicator for carotid artery plaques and thus, should be observed in patients with CHD.

Low-/high-density lipoprotein cholesterol ratio and carotid plaques in patients with coronary heart disease: a Chinese cohort study.

BACKGROUND: Evidence on the relationship between the low-/high-density lipoprotein cholesterol ratio (LDL-C/HDL-C) and carotid plaques remains limited. This study aimed to examine the association between LDL-C/HDL-C and carotid plaques in participants with coronary heart disease (CHD) and to further explore the extent to which a healthy lifestyle reduces the risk of LDL-C/HDL-C-related carotid plaques. METHODS: This large-scale and multi-centre retrospective study included 9426 CHD patients (aged 35-75 years) between January 1, 2014 and September 30, 2020. The LDL-C/HDL-C values were converted to the following tertiles: lowest (< 2.15), middle (2.15-3), and highest (> 3). Healthy lifestyle-related factors referred to whether or not the participant was a non-smoker and non-drinker. Participants were divided into an unfavourable group (those who did not adhere to healthy lifestyle factors), intermediate (only one unhealthy factor), and favourable (neither of the two unhealthy factors). Logistic regression was used for statistical analyses. RESULTS: Of the 9426 participants, 6989 (74.15%) CHD patients had carotid plaques. After adjustment for confounders, each unit increase in the LDL-C/HDL-C was significantly associated with carotid plaques (OR: 1.61; 95%CI: 1.43-1.84; P <  0.001). Multivariate logistic regression revealed that carotid plaques risk for the highest tertile (> 3) was 1.18 times that of the lowest quartile (< 2.15). Compared with an unfavourable lifestyle, an intermediate or a favourable lifestyle was associated with a significant 30% (OR: 0.70; 95%CI: 0.64-0.78; P <  0.001) or 67% (OR: 0.33; 95%CI: 0.29-0.37; P <  0.001) reduction in carotid plaques risk, respectively, among CHD patients with high LDL-C/HDL-C. There were significantly additive and multiplicative interactions between lifestyle and LDL-C/HDL-C with regards to carotid plaques. CONCLUSION: A high LDL-C/HDL-C is associated with a risk of carotid plaques developing in CHD patients. Adhering to a healthy lifestyle has additive beneficial effects on reducing the risk of carotid plaques, especially in relation to the highest LDL-C/HDL-C.

Establishment of a prediction model of changing trends in cardiac hypertrophy disease based on microarray data screening.

The aim of the present study was to construct a mathematical model to predict the changing trends of cardiac hypertrophy at gene level. Microarray data were downloaded from Gene Expression Omnibus database (accession, GSE21600), which included 35 samples harvested from the heart of Wistar rats on postoperative days 1 (D1 group), 6 (D6 group) and 42 (D42 group) following aorta ligation and sham operated Wistar rats, respectively. Each group contained six samples, with the exception of the samples harvested from the aorta ligated group after 6 days, where n=5. Differentially expressed genes (DEGs) were identified using a Limma package in R. Hierarchical clustering analysis was performed on common DEGs in order to construct a linear equation between the D1 and D42 groups, using linear discriminant analysis. Subsequent verification was performed using receiver operating characteristic (ROC) curve and the measurement data at day 42. A total of 319, 44 and 57 DEGs were detected in D1, D6 and D42 sample groups, respectively. AKIP1, ANKRD23, LTBP2, TGF-ß2 and TNFRSF12A were identified as common DEGs in all groups. The predicted linear equation between D1 and D42 group was calculated to be y=1.526×-186.671. Assessment of the ROC curve demonstrated that the area under the curve was 0.831, with a specificity and sensitivity of 0.8. As compared with the predictive and measurement data at day 42, the consistency of the two sets of data was 76.5%. In conclusion, the present model may contribute to the early prediction of changing trends in cardiac hypertrophy disease at gene level.