1.Influenza-associated intracranial aspergillosis a case report and literature review
SHI Dinghua ; XIONG Menglong ; HU Qiyao ; CHEN Chunyuan
China Tropical Medicine 2024;24(4):489-
To investigate the clinical features, early recognition and prognosis of influenza-associated intracranial aspergillosis. The clinical data of a child with influenza-related intracranial aspergillosis admitted to the Department of Pediatrics of the Third Xiangya Hospital of Central South University in 2022 were retrospectively analyzed. By searching CNKI, Wanfang Database, Web of Science, PubMed and other Chinese and English databases as of November 2023, literature was screened according to inclusion and exclusion criteria, and the clinical characteristics, diagnosis, treatment and prognosis of all influenza-related intracranial aspergillus disease were summarized. A total of 5 reports of 5 cases of influenza-associated aspergillosis were obtained, including 1 child patient and 1 child influenza-associated intracranial aspergillosis in this study, and a total of 6 influenza-associated aspergillosis patients. The clinical manifestations of the 6 patients were disturbance of consciousness, hemiplegia, pupil changes, behavioral abnormalities, epilepsy, etc. Most of the cases were diagnosed through pathology or autopsy to find pathogens. In this case, the pathogens were confirmed through metagenomic next-generation sequencing (mNGS). Antifungal drugs were the first choice for treatment. 66.7% of the surviving patients received surgical treatment, and the mortality rate of 6 patients reached 50.0%. Influenza-associated intracranial aspergillosis is rare, can occur in both children and adults, and has a poor prognosis. In the early stage of influenza, if there are neurological symptoms, screening for fungal infection should be conducted. Acer second generation sequencing can improve the diagnosis rate of intracranial aspergillosis.
2.Invasive renal angiomyolipoma combined with pseudoaneurysm formation:A case report and literature review
Mingli WU ; Qing ZHU ; Yue HU ; Qiyao LIU ; Lianjing ZHANG ; Dongyan YANG
Journal of Jilin University(Medicine Edition) 2024;50(1):254-259
Objective:To discuss the distinctive sonographic feature and the biological behavior of renal angiomyolipoma(RAML),and to provide the reference for the clinicians to make the accurate diagnosis of RAML.Methods:The clinical data of one patient with invasive classical RAML combined with pseudaneurysm formation were collected.The sonographic appearances were analyzed in conjunction with the pathological characteristics to clarify the biological behavior of RAML,and the relevant literatures were reviewed.Results:The patient,a 60-year-old female,visited the local hospital due to discomfort in the lumbar area,and received CT examination,and the CT examination results revealed a left renal mass,so the patient came to our hospital.The specialist clinical examinations and laboratory investigations were unremarkable.The ultrasound results indicated an enlarged left kidney with a cystic and solid mass at the upper pole,which featured pseudaneurysm formation(originating from the interlobar arteries);the enhanced CT image results suggested a high probability of upper pole renal carcinoma combined with aneurysmal formation within the tumor,alongside invasion into the left adrenal gland.The patient underwent laparoscopic radical left nephrectomy,and the postoperative pathology confirmed the diagnosis of invasive classical RAML.Conclusion:The classical RAML can exhibit the invasive biological behavior.The pseudaneurysm formation is a special sonographic manifestation of RAML,which can be challenging to differentiate from the other renal tumors.
3.One case of pancreatic head metastasis from colon cancer
Qiyao LIU ; Lianjing ZHANG ; Congmin WANG ; Yali XUE ; Zhiyu XIAO ; Yue HU ; Dongyan YANG
Chinese Journal of Endocrine Surgery 2024;18(3):463-464
Pancreatic metastases originating in colon cancer are very rare clinically, and there are few reports on their imaging manifestations. In this paper, it improves the diagnosis of the disease by reporting a case of pancreatic head metastases and focusing on the appearance of contrast-enhanced ultrasound.
4.Reform and reflection of teaching microbiology in English.
Yuanchan LUO ; Xiaoyan ZHANG ; Qiyao WANG ; Jiaofang HUANG ; Fengxian HU ; Shuhong GAO ; Ruifang YE ; Peng ZUO ; Yingping ZHUANG ; Hui WU
Chinese Journal of Biotechnology 2022;38(8):3099-3109
Microbiology is a key basic professional course for all the students specializing in biology, biotechnology and related majors. To date, microbiology is mainly taught in Chinese within colleges and universities in China. Development of a microbiology course that is taught in English may satisfy the diversified learning needs of the students and promote the "Double First-Class" initiative. We started to teach the microbiology course in English at the East China University of Science and Technology since 2016. This practice was associated with reform and innovation in the teaching methods and contents. The microbiology course taught in English greatly attracted the interest of the attending students and helped improve their professional English learning as well as scientific research. This course provided important support for fostering innovative professional first-class undergraduates under the context of the "Double First-Class" initiative.
China
;
Humans
;
Learning
;
Students
;
Universities
5.Effect of Ginkgo biloba extract on improving hepatic insulin resistance induced by arsenic exposure based on network pharmacology
Zhida HU ; Shiqing XU ; Ruru MENG ; Yanfeng JIA ; Qiyao ZHANG ; Bohao BIAN ; Shurui WANG ; Yang LIU ; Li WANG ; Yanrong GAO
Journal of Environmental and Occupational Medicine 2024;41(7):751-759
Background Arsenic exposure is a common and important environmental and occupational hazardous factor in China, and arsenic-induced insulin resistance (IR) has attracted widespread attention as a negative health outcome to the population. Objective To explore part of the mechanism of hepatic IR induced by arsenic exposure based on the peroxisome proliferators-activated receptors γ (PPARγ)/ glucose transporter 4 (GLUT4) pathway, and to investigate potential effects of Ginkgo biloba extract (GBE) on hepatic IR induced by arsenic exposure and associated mechanism of action. Methods The target of drug action was predicted by network pharmacology and verified by in vivo and in vitro experiments. In vivo experiments: 48 SPF C57BL/6J male mice were divided into 4 groups, including control group, 50 mg·L−1 NaAsO2 model group (NaAsO2), 50 mg·L−1 NaAsO2+10 mg·kg−1 GBE intervene group (NaAsO2+GBE), and 10 mg·kg−1 GBE group (GBE), 12 mice in each group. The animals were given free access to purified water containing 50 mg·L−1 NaAsO2, or given intraperitoneal injection of normal saline containing 10 mg·kg−1 GBE once per week. After 6 months of exposure, blood glucose detection, intraperitoneal glucose tolerance test (IPGTT), and insulin tolerance test (ITT) were performed. Serum and liver tissues were collected after the mice were neutralized, liver histopathological sections were obtained, serum insulin levels, liver tissue glycogen content, glucose content were detected by enzyme linked immunosorbent assay (ELISA), and the expression of PPARγ and GLUT4 proteins was detected by Western blot (WB). In vitro experiments: HepG2 cells were divided into 4 groups, including control group, 8 μmol·L−1 NaAsO2 group (NaAsO2), 8 μmol·L−1 NaAsO2 + 200 mg·L−1 GBE intervene group (NaAsO2+GBE), and 200 mg·L−1 GBE group (GBE). The levels of glycogen and glucose were detected by ELISA, and the expression of PPARγ and GLUT4 proteins was detected by WB. Results A strong binding effect between GBE and PPARγ was revealed by network pharmacology. In in vivo experiments, the NaAsO2 group exhibited an elevated blood glucose compared to the control group, and the NaAsO2+GBE group showed a decreased blood glucose compared to the NaAsO2 group (P<0.01). The histopathological sections indicated severe liver structural damage in the arsenic exposure groups (NaAsO2 group and NaAsO2+GBE group), with varying staining intensity, partial liver cell necrosis, and diffuse red blood cell appearance. Both results of in vitro and in vivo experiments showed a decrease in glycogen synthesis and glucose uptake in the NaAsO2 groups compared to the control groups, which was alleviated in the NaAsO2+GBE group (P<0.01). The results of WB revealed inhibited PPARγ expression and reduced GLUT4 levels on the cell membrane, and all these changes were alleviated in the NaAsO2+GBE group (P<0.01). Conclusion This study findings suggest that GBE antagonizes arsenic exposure-induced hepatic IR by regulating the PPARγ/GLUT4 pathway, indicating that GBE has a protective effect on arsenic exposure-induced hepatic IR, and PPARγ may be a potential therapeutic target for arsenic exposure-induced hepatic IR.
6.Mechanism of IGF2BP2 regulation of PPAR-γ/GLUT4 pathway in insulin resistance induced by sodium arsenite exposure in HepG2 cells
Shiqing XU ; Zhida HU ; Qiyao ZHANG ; Siqi ZHAO ; Yujie WANG ; Xiaohui WANG ; Teng MA ; Li WANG
Journal of Environmental and Occupational Medicine 2025;42(4):400-407
Background Arsenic is an environmentally harmful substance that causes hepatic insulin resistance and liver damage, increasing the risk of type 2 diabetes mellitus. Objective To explore whether the insulin-like growth factor 2 mRNA binding protein 2 (IGF2BP2) is involved in insulin resistance in HepG2 cells after arsenic exposure through the peroxisome-proliferator-activated receptor γ (PPAR-γ) / glucose transporter 4 (GLUT4) pathway. Methods Cell viability was determined using cell counting kit 8 (CCK8) and an appropriate NaAsO2 infection dose was determined. A cellular arsenic exposure model of HepG2 cells was established by four concentrations of NaAsO2 solution for 24 h (the experiment was divided into four groups: 0, 2, 4, and 8 μmol·L−1); HepG2 cells were firstly treated with pcDNA3.1-IGF2BP2 and pcDNA3.1-NC respectively for 6 h, then with 8 μmol·L−1 NaAsO2 for 24 h to establish a IGF2BP2 overexpression cell model (the experiment was divided into 4 groups: control, NaAsO2, NaAsO2+pcDNA3.1-IGF2BP2, and NaAsO2+pcDNA3.1-NC); finally the cells were subject to 100 nmol·L−1 insulin stimulation for 30 min. Glycogen and glucose in HepG2 cells were determined by glycogen and glucose assay kits; mRNA expression levels of IGF2BP2 were measured by quantitative real-time PCR; protein expression levels of IGF2BP2, PPAR-γ, and GLUT4 in HepG2 were detected by Western blot (WB); and the binding of IGF2BP2 to PPAR-γ and PPAR-γ to GLUT4 was verified by co-immunoprecipitation (CO-IP) experiment. Results The results of CCK8 experiment showed a dose-effect relationship between NaAsO2 concentration and cell viability. When the concentration of NaAsO2 was ≥4 μmol·L−1 , the cell viabilities were lower than that of the control group (P <0.05). With the increasing dose of NaAsO2 infection, reduced glucose consumption and glycogen levels in HepG2 cells were found in the 2, 4, and 8 μmol·L−1 NaAsO2 treatment groups compared to the control group (P <0.05). The difference between the mRNA expression level of IGF2BP2 in the HepG2 cells treated with 4 or 8 μmol L−1 NaAsO2 and the control group was significant (P <0.05). In the IGF2BP2 overexpression cell model, compared with the control group, glucose consumption and glycogen levels were lowered in the NaAsO2 group (P <0.05), the mRNA expression level of IGF2BP2 and the protein expression levels of IGF2BP2, PPAR-γ, and GLUT4 in the cell membrane were all decreased (P <0.05). Compared with the NaAsO2 group, the glucose consumption and glycogen levels were increased in the NaAsO2+pcDNA3.1-IGF2BP2 group (P <0.05), and the mRNA expression level of IGF2BP2 and the protein expression levels of IGF2BP2, PPAR-γ, and GLUT4 in the cell membrane were all increased (P <0.05). The results of CO-IP experiments showed that IGF2BP2 interacted with PPAR-γ as well as PPAR-γ with GLUT4 protein. Conclusion IGF2BP2 is involved in arsenic exposure-induced insulin resistance in HepG2 cells by acting on the PPAR-γ/GLUT4 pathway.