Cell death is divided into uncontrolled accidental cell death (ACD) and controllable regulatory cell death (RCD). RCD is also known as programmed cell death (PCD) under physiological conditions. PANoptosis is a recently discovered inflammatory RCD pathway regulated by a cytoplasmic polymeric protein complex called PANoptosome. This complex has the key features of apoptosis, pyrodeath, and/or necrotic apoptosis, but cannot be explained by any of these 3 RCD pathways alone. However, the specific role of PANoptosis in human tumor cells remains to be clarified. At present, the understanding of the molecular mechanism of PANoptosis and the assembly of PANoptosome is very limited, but several important regulatory targets have been identified such as melanoma deficiency factor 2 (AIM2), caspase family members(including CASP3, CASP6, and CASP8), Z-DNA-binding protein 1 (ZBP1), receptor-interacting protein kinase 1/3 (RIPK1/3) and interferon regulatory factor 1 (IRF1). The discovery of these markers indicates a breakthrough for the optimization of cancer treatment strategies.

Cell death is divided into uncontrolled accidental cell death (ACD) and controllable regulatory cell death (RCD). RCD is also known as programmed cell death (PCD) under physiological conditions. PANoptosis is a recently discovered inflammatory RCD pathway regulated by a cytoplasmic polymeric protein complex called PANoptosome. This complex has the key features of apoptosis, pyrodeath, and/or necrotic apoptosis, but cannot be explained by any of these 3 RCD pathways alone. However, the specific role of PANoptosis in human tumor cells remains to be clarified. At present, the understanding of the molecular mechanism of PANoptosis and the assembly of PANoptosome is very limited, but several important regulatory targets have been identified such as melanoma deficiency factor 2 (AIM2), caspase family members(including CASP3, CASP6, and CASP8), Z-DNA-binding protein 1 (ZBP1), receptor-interacting protein kinase 1/3 (RIPK1/3) and interferon regulatory factor 1 (IRF1). The discovery of these markers indicates a breakthrough for the optimization of cancer treatment strategies.

Objective:To investigate the association of surrogate indexes of insulin resistance with the risk of nonalcoholic fatty liver disease(NAFLD)and advanced liver fibrosis in newly diagnosed patients with type 2 mellitus.Methods:A total of 429 newly diagnosed type 2 diabetic patients hospitalized in the Department of Endocrinology and Metabolism, Shanghai Ninth People′s Hospital, Shanghai Jiao Tong University School of Medicine from June 2018 to June 2020 were included. The patients were divided into NAFLD group( n=263)and non-NAFLD group( n=166)according to the results of abdominal ultrasound, NAFLD patients were divided into advanced liver fibrosis group( n=33)and non-advanced liver fibrosis group( n=230)according to the NAFLD fibrosis score(NFS). The correlation of the triglyceride/high density lipoprotein-cholesterol ratio(TG/HDL-C), triglyceride glucose index(TyG), visceral adiposity index(VAI), triglyceride glucose-body mass index(TyG-BMI), homeostasis model assessment of insulin resistance index(HOMA-IR)with NAFLD and the occurrence of advanced liver fibrosis were analyzed. Results:The prevalence of NAFLD in newly diagnosed type 2 diabetic patients was 61.3%, and the prevalence of advanced liver fibrosis was 12.5%. After adjusting the potential confounders, multivariate logistic regression analysis showed that TG/HDL-C, TyG, VAI, TyG-BMI, and HOMA-IR were independently and positively correlated with NAFLD, and only TyG-BMI was independently and positively correlated with advanced liver fibrosis( OR=1.021, 95% CI 1.009-1.034, P<0.01). The receiver operating characteristic analysis showed that the area under the curue of TyG-BMI was more than those of TG/HDL-C, TyG, VAI and HOMA-IR for predicting the occurrence of NAFLD in newly diagnosed type 2 diabetic patients(0.83 vs 0.73, 0.74, 0.73, 0.67, P<0.01), but had no predictive value for advanced liver fibrosis. Conclusion:TyG-BMI is superior to TG/HDL-C, TyG, VAI and HOMA-IR for predicting the occurrence of NAFLD in newly diagnosed type 2 diabetic patients, and it is also an independent risk factor for advanced liver fibrosis.

Objective To investigate the clinical and imaging characteristics of phosphaturic mesenchymal tumor and improve the clinical diagnosis. Methods From November 2014 to September 2017, 22 patients with pathologically confirmed diagnosis as phosphaturic mesenchymal tumor (PMT) were retrospectively analyzed, including 12 males and 10 females, age ranged from 30-72 years, mean (47 ± 11) years old. The clinical data, laboratory tests [serum calcium, phosphorus, alkaline phosphatase, parathyroid hormone and 1, 25- (OH) 2 D] and imaging examinations (X-ray, CT, MRI, nuclide) were collected and explored. Sixteen patients underwent SPECT scan and seven underwent PET/CT scan. Twenty patients had X-ray, eighteen patients had CT and 12 patients had MRI with enhancement. Results All patients suffered from diffuse pain for one to fifteen years, especially in lower back and lower extremities. All patients were found with low serum phosphorus, normal serum calcium. Twenty-one patients were found with elevated alkaline phosphatase, 16 with increased parathyroid hormone and 15 with decreased 1, 25 - (OH) 2 D. Thirteen lesions were located in the medullary cavity, seven in the soft tissue and two in the sinuses. Nineteen cases showed varying degrees of trabecular bone sparse, osteoporosis and osteomalacia on X-ray;There were 15 cases of multiple pseudo-fractures, including four cases of pelvic fracture complicated with femoral fracture, six cases of single fracture of pelvis, four cases of femur and one case of fibula. And seven cases showed multiple vertebral compression fractures. Thirteen lesions showed soft-tissue density and four in the medullary cavity showed high density on CT scan. The lesions presented low signal intensity on T1WI,high or low signal intensity on T2WI FLAIR and obviously enhanced in 12 patients who underwent MRI enhancement. Conclusion For patients with decreased serum phosphorus, elevated alkaline phosphatase, bone softening and fracture, octreotide or other nuclides should be primary imaging modality for confirming the location of the lesion. CT and MRI can further evaluate the nature of the lesion and improve diagnostic accuracy.

Objective To determine the triterpenoid content in Loquat leaf by using HPLC method and to explore the feasibility of ursolic acid and oleanolic acid as the quantitative markers for determination of Loquat leaf and its preparations.Methods Two desugaring methods of Loquat leaf extracts were compared.The contents of ursolic acid and oleanolic acid in Loquat leaf as well as preparations were measured based on a system of HPLC,with a Dumas Diamonsil C18 column (250 mm×4.6 mm,5 μm) was used as analytical column.The mobile phase was consisted of acetonitrile-0.1% phosphoric acid (95∶5) with the flow rate of 0.5 mL·min-1.The column temperature was 30 ℃,the injection volume was 10 μL, the detective wavelength was 210 nm.Results Ursolic acid and oleanolic acid were measured in both Loquat leaf and its preparations,and their contents were fairy stable and comparable.Conclusion Ursolic acid and oleanolic acid can be served as quantitative markers for the determination of Loquat leaf and its preparations.

Objective To investigate the interaction between uropathogenic Escherichia coli (UPEC) and host uroepithelial cells, define the role uroepithelial cells play in initiating and modulating the host response to infection with UPEC strain. Methods The human bladder transitional epithelial EJ cells were evaluated for their capacities to allow the adherence and invasion by UPEC132, a clinical strain isolated from Tianjin, China, and a cDNA microarray for 22 000 human genes was used to identify the gene expression differences between EJ cells infected with UPEC132 and uninfected EJ cells. Results Microscope observation showed that UPEC132 could adhere to EJ cells with the adherence rate of (73.20 ± 5.26)%. And visualization by confocal microscope revealed that this microorganism could be seen within the cells. EJ cells infected with UPEC132 changed mRNA expression of a total of 29 genes, including 28 genes up-regulated and 1 gene down-regulated. Of these, regulators of growth and proliferation, cytokines, and modulators of apoptotic responses were the most prominent. Conclusion The gene expression profiling of EJ cells is affected by the infection of UPEC strain. The differentially expressed genes may contribute to further investigate the interaction of UPEC and uroepithelial cells.