Objective:To investigate the effects of Xiaoyu-Jiangzhi capsules on blood lipid, carotid artery atherosclerosis (CAA) and plaque in apolipoprotein E knockout (ApoE -/-) mice. Methods:The ApoE -/- mice were fed with high-fat food to establish carotid atherosclerosis model. The ApoE -/- mice were randomly by weight divided into model group, Atorvastatin group, low- and high-dose Xiaoyu-Jiangzhi capsules group. The C57BL/6cnc mice were used as control group and fed with normal diet. The Atorvastatin group was given atorvastatin suspension 1.3 mg/kg, low and high dose groups were given Xiaoyu-Jiangzhi capsule suspension 325 and 975 mg/kg, and the control group and model group were given equal volume of distilled water. The mice were gavaged with 0.1 ml/10 g body weight, once a day, and the weight of mice was recorded weekly. After 12 weeks of continuous intragastric administration, the blood lipid and liver /body weight index of the mice were measured. Carotid arteries were sliced to conduct oil red O staining and VG staining for the pathological analysis. Results:After 12 weeks of drug administration, the weight of mice in the high-dose group was significantly lower than the model group. The level of TC (25.92 ± 4.21 mmol/L vs. 30.39 ± 4.67 mmol/L) and LDL-C (7.97 ± 2.14 mmol/L vs. 10.26 ± 1.97 mmol/L) in the high-dose group significantly decreased ( P<0.05), the level of HDL-C in the low and high-dose group significantly increased ( P<0.05). The pathological results showed that after 12 weeks of administration, the carotid artery lipid deposition blockage rate in the Atorvastatin group and the high dose group were significantly smaller than the model group( P<0.05), and no vascular plaque has been formed. Conclusion:The Xiaoyu-Jiangzhi capsules could reduce LDL-C, increase HDL-C levels, reduce the constriction of arterial stenosis and slow down the formation process of carotid plaque.

Objective:To summarize the clinical and electrophysiological characteristics of epilepsy patients with fixation-off sensitivity (FOS).Methods:Using "fixation-off sensitivity" and "epilepsy" as search terms, data were retrieved from the Electroencephalogram Monitoring Center Database of Xijing Hospital, Air Force Military Medical University. Information was collected on epilepsy patients with FOS who were seen at the Xijing Hospital Electroencephalogram Monitoring Center from March 2019 to May 2023. A retrospective analysis of video electroencephalograms and clinical information was conducted, along with follow-up. Single factor analysis and multi-factor Logistic regression analysis were used to analyze the risk factors affecting the prognosis of the patients.Results:A total of 78 patients met the inclusion criteria, including 43 females and 35 males; the age at first epilepsy onset was 12.00 (8.00, 15.25) years. Among these 78 patients, 46 were diagnosed with genetic generalized epilepsy, 11 with self-limited focal epilepy, 9 with familial cortical myoclonic tremor with epilepsy, 7 with developmental and epileptic encephalopathy, 3 with symptomatic epilepsy, and 2 with progressive myoclonic epilepsy. The fixation-off induction trial most commonly triggered seizures in epilepsy with eyelid myoclonia (EEM) patients, with eyelid myoclonia being the most common type of seizure. Twenty-five epilepsy patients with FOS showed a positive photoparoxysmal response, of whom 6 experienced photo-convulsive response. Sixty-eight patients completed follow-up with comprehensive clinical data. At the last follow-up, 45 patients had been free from tonic-clonic seizures for at least one year. A history of febrile seizures ( OR=20.559, 95% CI 2.179-193.997, P=0.008) and cognitive decline ( OR=3.752, 95% CI 1.118-12.588, P=0.032) were identified as risk factors for poor prognosis in epilepsy patients with FOS. The age of first epilepsy onset, the number of anti-seizure medications, and the intermittent photo stimulation trial results had no correlation with prognosis. Conclusions:FOS is more common in female epilepsy patients and can be observed in both generalized and focal epilepsy syndromes. EEM patients are prone to seizures during fixation-off induction trial, and the most common type of seizures is eyelid myoclonus seizure. Patients with epilepsy with FOS who have a history of febrile seizures and cognitive impairment tend to have poor prognosis.

BACKGROUND: Previous research demonstrated that a homozygous mutation of g.136372044G>A (S12N) in caspase recruitment domain family member 9 ( CARD9 ) is critical for producing Aspergillus fumigatus -induced ( Af -induced) T helper 2 (T H 2)-mediated responses in allergic bronchopulmonary aspergillosis (ABPA). However, it remains unclear whether the CARD9S12N mutation, especially the heterozygous occurrence, predisposes the host to ABPA. METHODS: A total of 61 ABPA patients and 264 controls (including 156 healthy controls and 108 asthma patients) were recruited for sequencing the CARD9 locus to clarify whether patients with this heterozygous single-nucleotide polymorphisms are predisposed to the development of ABPA. A series of in vivo and in vitro experiments, such as quantitative real-time polymerase chain reaction, flow cytometry, and RNA isolation and quantification, were used to illuminate the involved mechanism of the disease. RESULTS: The presence of the p.S12N mutation was associated with a significant risk of ABPA in ABPA patients when compared with healthy controls and asthma patients, regardless of Aspergillus sensitivity. Relative to healthy controls without relevant allergies, the mutation of p.S12N was associated with a significant risk of ABPA (OR: 2.69 and 4.17 for GA and AA genotypes, P = 0.003 and 0.029, respectively). Compared with patients with asthma, ABPA patients had a significantly higher heterozygous mutation (GA genotype), indicating that p.S12N might be a significant ABPA-susceptibility locus ( aspergillus sensitized asthma: OR: 3.02, P = 0.009; aspergillus unsensitized asthma: OR: 2.94, P = 0.005). The mutant allele was preferentially expressed in ABPA patients with heterozygous CARD9S12N , which contributes to its functional alterations to facilitate Af -induced T H 2-mediated ABPA development. In terms of mechanism, Card9 wild-type ( Card9WT ) expression levels decreased significantly due to Af -induced decay of its messenger RNA compared to the heterozygous Card9S12N . In addition, ABPA patients with heterozygous CARD9S12N had increased Af -induced interleukin-5 production. CONCLUSION Our study provides the genetic evidence showing that the heterozygous mutation of CARD9S12N , followed by allele expression imbalance of CARD9S12N , facilitates the development of ABPA.
Humans ; Aspergillosis, Allergic Bronchopulmonary/complications* ; Aspergillus fumigatus/genetics* ; Asthma/genetics* ; Aspergillus ; Mutation/genetics* ; CARD Signaling Adaptor Proteins/genetics*