The rapid development of artificial intelligence (AI), especially generative AI (GenAI), has already brought, and will continue to bring, revolutionary changes to our daily production and life, as well as create new opportunities and challenges for diagnostic and therapeutic practices in the medical field. Haihe Hospital of Tianjin University collaborates with the National Supercomputer Center in Tianjin, Tianjin University, and other institutions to carry out research in areas such as smart healthcare, smart services, and smart management. We have conducted research and development of a full-process disease diagnosis and treatment assistance system based on GenAI in the field of smart healthcare. The development of this project is of great significance. The first goal is to upgrade and transform the hospital's information center, organically integrate it with existing information systems, and provide the necessary computing power storage support for intelligent services within the hospital. We have implemented the localized deployment of three models: Tianhe "Tianyuan", WiNGPT, and DeepSeek. The second is to create a digital avatar of the chief physician/chief physician's voice and image by integrating multimodal intelligent interaction technology. With generative intelligence as the core, this solution provides patients with a visual medical interaction solution. The third is to achieve deep adaptation between generative intelligence and the entire process of patient medical treatment. In this project, we have developed assistant tools such as intelligent inquiry, intelligent diagnosis and recognition, intelligent treatment plan generation, and intelligent assisted medical record generation to improve the safety, quality, and efficiency of the diagnosis and treatment process. This study introduces the content of a full-process disease diagnosis and treatment assistance system, aiming to provide references and insights for the digital transformation of the healthcare industry.
Artificial Intelligence ; Humans ; Delivery of Health Care ; Generative Artificial Intelligence

Objective:To discuss the protective effect of ginsenoside Rh1(G-Rh1)on kidney injury in the diabetic mellitus(DM)mice,and to clarify its mechanism.Methods:The diabetic kidney disease(DKD)model was prepared by using the high-fat,high-sugar diet combined with intraperitoneal injection of streptozotocin(STZ).A total of 48 C57/BL6 model mice were randomly divided into model group,nuclear factor erythroid 2-related factor 2(Nrf2)inhibitor ML385 group(ML385 group)(30 mg·kg-1),G-Rh1 group(30 mg·kg-1),and G-Rh1+ML385 group(30 mg·kg-1 G-Rh1+30 mg·kg-1 ML385),and there were 12 mice in each group.Additionally,12 C57/BL6 mice were selected as control group.After treated for 8 weeks,automatic analyzer was used to detect the levels of fasting blood glucose(FBG),blood urea nitrogen(BUN),and serum creatinine(Scr)in serum of the mice in various groups,as well as 24 h urinary protein(24 h UP)levels in urine,and the kidney index was calculated;kits were used to detect the activities of superoxide dismutase(SOD)and lactate dehydrogenase(LDH),and the levels of malondialdehyde(MDA)in kidney tissue of the mice in various groups;Western blotting method was used to detect the expression levels of Nrf2 and heme oxygenase-1(HO-1)proteins in kidney tissue of the mice in various groups.Results:Compared with control group,the levels of FBG and kidney indexes in serum of the mice in model group,ML385 group,and G-Rh1+ML385 group were significantly increased(P<0.01),and the level of FBG in serum of the mice in G-Rh1 group was significantly increased(P<0.01);compared with model group,the kidney index of the mice in ML385 group was significantly increased(P<0.05),while the levels of FBG and kidney index of the mice in G-Rh1 group were significantly decreased(P<0.05 or P<0.01);compared with G-Rh1 group,the level of FBG and kidney index of the mice in G-Rh1+ML385 group were significantly increased(P<0.01).Compared with control group,the levels of BUN and Scr in serum,and 24 h UP in urine of the mice in model group,ML385 group,G-Rh1 group,and G-Rh1+ML385 group were significantly increased(P<0.01);compared with model group,the level of BUN in serum and 24 h UP in urine of the mice in ML385 group were significantly increased(P<0.05),while the levels of BUN and Scr in serum,and 24 h UP in urine of the mice in G-Rh1 group were significantly decreased(P<0.01);compared with G-Rh1 group,the levels of BUN and Scr in serum,and 24 h UP in urine of the mice in G-Rh1+ML385 group were significantly increased(P<0.01).Compared with control group,the activities of SOD in kidney tissue of the mice in model group,ML385 group,G-Rh1 group,and G-Rh1+ML385 group were significantly decreased(P<0.01),while the levels of MDA and LDH activities were significantly increased(P<0.01);compared with model group,the activity of SOD in kidney tissue of the mice in ML385 group was significantly decreased(P<0.05),and the level of MDA was significantly increased(P<0.05);the activity of SOD in kidney tissue of the mice in of G-Rh1 group was significantly increased(P<0.01),and the level of MDA and activity of LDH were significantly decreased(P<0.01);compared with G-Rh1 group,the activity of SOD in kidney tissue of the mice in G-Rh1+ML385 group was significantly decreased(P<0.01),and the level of MDA and activity of LDH were significantly increased(P<0.01).Compared with control group,the expression levels of Nrf2 and HO-1 proteins in kidney tissue of the mice in model group,ML385 group,G-Rh1 group,and G-Rh1+ML385 group were significantly decreased(P<0.05 or P<0.01);compared with model group,the expression levels of Nrf2 and HO-1 proteins in kidney tissue of the mice in ML385 group and G-Rh1+ML385 group were significantly decreased(P<0.05),while the expression levels of Nrf2 and HO-1 proteins in kidney tissue of the mice in G-Rh1 group were significantly increased(P<0.01);compared with G-Rh1 group,the expression levels of Nrf2 and HO-1 proteins in kidney tissue of the mice in G-Rh1+ML385 group were significantly decreased(P<0.01).Conclusion:Ginsenoside Rh1 reduces the oxidative stress and improves the kidney function,providing protective effects on kidney injury in the DM mice,and its mechanism may be related to the activation of the Nrf2/HO-1 signaling pathway.

A 67-year-old female patient was treated with oral 4 Panlongqi tablets thrice daily for strain of lumbar muscles. The patient developed nausea and poor appetite after 3 days of administration, followed by discharging strong brown urine and clay-colored stools. After 15 days of using the drug, she developed yellow staining of the skin and sclera, and itching appeared throughout the body. Laboratory tests showed alanine aminotransferase (ALT) 304 U/L, aspartate aminotransferase (AST) 168 U/L, alkaline phosphatase (ALP) 463.6 U/L, gamma glutamyltransferase (GGT) 1 332.3 U/L, total bilirubin (TBil) 110.5 μmol/L, and direct bilirubin (DBil) 92.3 μmol/L. After excluding viral hepatitis and biliary obstruction, drug-induced liver injury was diagnosed. Panlongqi tablets were stopped, and magnesium isoglycyrrhizinate, polyene phosphatidylcholine, ursodeoxycholic acid, and methylprednisolone were given. The patient′s discomfort symptoms were gradually eased and liver function was gradually improved. After 14 days of treatments, percutaneous liver biopsy under color doppler ultrasound was performed, and she was diagnosed as acute cholestatic hepatitis with mild fibrosis in the portal area, possibly caused by drug. After 16 days of treatments, the medication was switched to oral hepatoprotective drugs for 2 weeks. One week after stopping treatments, the patient had no discomfort and the color of skin and sclera was normal. The liver function was normal, showing ALT 31 U/L, AST 25 U/L, ALP 83.9 U/L, GGT 37.0 U/L, TBil 19.8 μmol/L, and DBil 7.3 μmol/L.

A 67-year-old female patient was treated with oral 4 Panlongqi tablets thrice daily for strain of lumbar muscles. The patient developed nausea and poor appetite after 3 days of administration, followed by discharging strong brown urine and clay-colored stools. After 15 days of using the drug, she developed yellow staining of the skin and sclera, and itching appeared throughout the body. Laboratory tests showed alanine aminotransferase (ALT) 304 U/L, aspartate aminotransferase (AST) 168 U/L, alkaline phosphatase (ALP) 463.6 U/L, gamma glutamyltransferase (GGT) 1 332.3 U/L, total bilirubin (TBil) 110.5 μmol/L, and direct bilirubin (DBil) 92.3 μmol/L. After excluding viral hepatitis and biliary obstruction, drug-induced liver injury was diagnosed. Panlongqi tablets were stopped, and magnesium isoglycyrrhizinate, polyene phosphatidylcholine, ursodeoxycholic acid, and methylprednisolone were given. The patient′s discomfort symptoms were gradually eased and liver function was gradually improved. After 14 days of treatments, percutaneous liver biopsy under color doppler ultrasound was performed, and she was diagnosed as acute cholestatic hepatitis with mild fibrosis in the portal area, possibly caused by drug. After 16 days of treatments, the medication was switched to oral hepatoprotective drugs for 2 weeks. One week after stopping treatments, the patient had no discomfort and the color of skin and sclera was normal. The liver function was normal, showing ALT 31 U/L, AST 25 U/L, ALP 83.9 U/L, GGT 37.0 U/L, TBil 19.8 μmol/L, and DBil 7.3 μmol/L.

Objective:To investigate the effect of Stigma Maydis Palysaccharide(SMPS)on ATP synthesis in kidney mitochondria of D-galactose-induced aging mice, and to clarify its possible mechanism.Methods:The aging mouse model was established by subcutaneous injection of D-galactose solution in the back of the neck.The 48 SPF male mice were randomly divided into normal control group(control group), D-galactose model group(D-Gal group), SMPS low-dose group and SMPS high-dose group(n=12 for each). The control group was subcutaneously injected with 150 mg/kg normal saline on the back of the neck every day, while the other three groups were subcutaneously injected with 150 mg/kg of D-gal solution on the back of the neck every day.SMPS-L and-H dose groups were given 30 mg/kg and 60 mg/kg of SMPS solution by gavage at the same day of D-Gal injection.The control group and D-GAL group were given the same volume of normal saline daily by gavage for 42 days.Blood samples were collected from the eyeball under general anesthesia after 42 days of intervention for the detection of serum levels of superoxide dismutase(SOD), glutathione peroxidase(GSH-Px)and MDA.After harvesting the kidney tissue, various tests were used to detect ATP content, the mRNA expression levels and protein expression levels in kidney.Luciferase assay was used to detect ATP content in renal tissue.Real-time fluorescent quantitative PCR was used to detect the mRNA expression levels of succinate dehydrogenase(SDH)of complex Ⅱ, cytochrome C reductase(Cycs)of complex Ⅲ, complex Ⅳ(COXⅣ)and ATP5b in ATP synthase in mitochondrial oxidative respiratory chain.Western blot was used to detect the expression levels of mitochondrial fusion protein 2(MFN2), dynamin-related protein1(DRP1)and mitochondrial autophagy related protein P62 in renal tissues of each group.Results:Compared with control group, the activities of serum of SOD(116.53±10.01)U/mg and GSH-Px(127.58±8.74)μmol/L were significantly decreased in D-GAL group(both P< 0.01), and serum MDA content(15.42±0.91)μmol/L increased significantly in D-GAL group( P<0.01). Compared with D-GAL group, the activities of SOD(152.80±9.29)U/mg and GSH-Px(274.07±10.73)μmol/L were significantly increased in SMPS intervention group( P< 0.01), while the MDA content(8.10±0.66)μmol/L decreased significantly in SMPS intervention group( P< 0.01). Compared with control group, the content of ATP(178±4)10 -4 μmol in D-gal group was significantly decreased( P<0.01), the mRNA expression levels of SDH, Cycs and COXⅣ were not significantly changed in D-gal group, and the mRNA expression level of ATP5b(0.67±0.01)was down-regulated in D-gal group( P<0.01), the expression of MFN2 protein(0.29±0.02)was significantly decreased in D-gal group( P<0.01), and the expression of DRP1 and P62 protein(0.31±0.02 and 0.21±0.01)was significantly increased in D-gal group(both P<0.01). Compared with the D-gal group, the ATP content(193±1)10 -4 μmol in the kidney tissue of the mice was significantly increased in SMPS intervention group( P< 0.01), and the ATP5b mRNA expression and MFN2 protein expression(0.87±0.05 and 0.71±0.08)were significantly increased in SMPS intervention group(both P< 0.01), DRP1 and P62 protein expressions(0.20±0.01 and 0.10±0.01)were significantly down-regulated in in SMPS intervention group(both P< 0.01). Conclusions:SMPS can improve the mitochondrial dynamic homeostasis disorder in aging mice by increasing the activity of antioxidant enzymes, up-regulating the expression of ATP5b mRNA and MFN2 protein, down-regulating the expression of DRP1 and P62 protein, and promoting the generation of mitochondrial ATP in D-gal-induced aging mice kidney tissue.

Genomic studies of cancer cell alterations,such as mutations,copy number variations(CNVs),and translocations,greatly promote our understanding of the genesis and development of cancers.However,the 3D genome architecture of cancers remains less studied due to the complexity of cancer genomes and technical difficulties.To explore the 3D genome structure in clin-ical lung cancer,we performed Hi-C experiments using paired normal and tumor cells harvested from patients with lung cancer,combining with RNA sequenceing analysis.We demonstrated the feasibility of studying 3D genome of clinical lung cancer samples with a small number of cells(1×104),compared the genome architecture between clinical samples and cell lines of lung cancer,and identified conserved and changed spatial chromatin structures between normal and cancer sam-ples.We also showed that Hi-C data can be used to infer CNVs and point mutations in cancer.By integrating those different types of cancer alterations,we showed significant associations between CNVs,3D genome,and gene expression.We propose that 3D genome mediates the effects of cancer genomic alterations on gene expression through altering regulatory chromatin structures.Our study highlights the importance of analyzing 3D genomes of clinical cancer samples in addition to cancer cell lines and provides an integrative genomic analysis pipeline for future larger-scale studies in lung cancer and other cancers.

Objective:To establish a direct dilution-inductively coupled plasma mass spectrometry method for the determination of manganese in urine.Methods:Using 1% nitric acid solution as diluent, the urine dilution factor and internal standard elements were determined by single factor rotation experiment. The linear range, correlation coefficient, precision, accuracy and detection limit of the direct dilution-inductively coupled plasma mass spectrometry for the determination of manganese in urine were evaluated.Results:The linear range of this method was 0.0-20 μg/L, the correlation coefficient was 0.999 9, the detection limit was 0.02 μg/L, the recoveries were 84.65%-103.40%, the relative standard deviations were 0.26%-8.17%.Conclusion:This method has the advantages of simple operation, high sensitivity and low detection limit. It can be used for the determination of urine manganese at the same time with other elements. It is suitable for the determination of urine manganese in workers and ordinary people.

Objective:To establish a direct dilution-inductively coupled plasma mass spectrometry method for the determination of manganese in urine.Methods:Using 1% nitric acid solution as diluent, the urine dilution factor and internal standard elements were determined by single factor rotation experiment. The linear range, correlation coefficient, precision, accuracy and detection limit of the direct dilution-inductively coupled plasma mass spectrometry for the determination of manganese in urine were evaluated.Results:The linear range of this method was 0.0-20 μg/L, the correlation coefficient was 0.999 9, the detection limit was 0.02 μg/L, the recoveries were 84.65%-103.40%, the relative standard deviations were 0.26%-8.17%.Conclusion:This method has the advantages of simple operation, high sensitivity and low detection limit. It can be used for the determination of urine manganese at the same time with other elements. It is suitable for the determination of urine manganese in workers and ordinary people.

OBJECTIVE To investigate the effect of prenatal nicotine exposure on cardiac ejection function and myocardial fibrosis of the offspring of rats.METHODS Pregnant rats were sc given nicotine 6.0 mg· kg-1,once daily for 17 d.The body mass and heart mass of the offspring were detected at the 21th day of gestation,and 15 and 90 d after birth.Heart rate of 90 d offspring was recorded by ECG,and cardiac functions were detected by Doppler ultrasonography,including cardiac output (CO),stroke volume (SV),ejection fraction (EF),left ventricular long axis shortening fraction (FS),interventricular septum diastolic diameter (IVSd) and left ventricular posterior wall diastolic diameter (LVPWd).The myocardial ultrastructure was detected under an electron microscope.Masson staining was used to detect the myocardial collagen fiber deposition.The level of collagen protein type Ⅰ in heart tissue was detected by radioimmunoassay.RESULTS Compared with control group,prenatal nicotine exposure resulted in a decrease of heart mass and body mass in groups of 21 d fetal rats and 15 d offspring(P＜0.05,P＜0.01),but had no effect on the 90 d offspring.Compared with the normal control group,the heart rate of 90 d offspring increased [366+10 vs (418+10) min-1] (P＜0.05),CO,FS and EF decreased (P＜0.01),and IVSd and LVPWd increased (P＜0.05,P＜0.01).Electron microscopy revealed that in the heart of nicotine 90 d offspring,myocardial fiber arrangement was loosened and confused,while extracellular matrix increased.Masson staining showed collagen deposited in the myocardium.The level of collagen type Ⅰ in heart tissue increased [0.59±0.09 vs (0.40±0.05) tμg·g-1 tissue] (P＜0.01).CONCLUSION Prenatal nicotine exposure induces the increased level of cardiac collagen type Ⅰ,myocardial fibrosis and decrease of cardiac ejection function in adult offspring,which may lead to increased susceptibility to cardiovascular diseases.

Objective Salidroside is a major active component of integripetal rhodiola herbal medicine, which has a significant activity against hypoxia and ischemia.This study was to investigate the effects of side chain carbon losssalidroside analogues (N04) on the expressions of HIF-1α-related factors in the hypoxia-injured EAhy926 human vascular endothelial cells.Methods EAhy926 human umbilical vein endothelial cells in the logarithmic growth phase were randomly divided into a normal control, a hypoxia model control, a salidroside, a high-dose N04, a medium-dose N04, and a low-dose N04 group.The hypoxia model was established by depriving the culture medium of sugar and serum and culturing the EAhy926 cells in an environment of 95%N2+5%CO2 for 2 hours, followed by intervention with salidroside at 1×10-6 mol/L and N04 at 1×10-6, 1×10-7, and 1×10-8 mol/L, respectively.Then, the activity of the cells was detected by MTT assay, their LDH activity examined by spectrophotometry, the mRNA expressions of HIF-1α and VEGF measured by RT-PCR, the protein expressions of HIF-1α, VEGF and pVHL determined by Western blot, and the activity of eNOS measured by ELISA.Results Compared with the normal control group, the hypoxia model cells showed significantly reduced activity (0.51±0.05 vs 0.27±0.02, P<0.01), an elevated LDH level ([6.65±1.43] vs [78.82±2.33] U/L, P<0.01), and decreased eNOS activity ([1.56±0.23] vs [1.16±0.20] U/100 mL, P<0.01).In comparison with the hypoxia model group, the cells treated with high-, medium-, and low-dose N04 exhibited remarkably increased activity (0.27±0.02 vs 0.0.42±0.05, 0.40±0.03 and 0.37±0.04, P<0.01), a reduced LDH level ([78.82±2.33] vs [53.05±3.90], [58.42±4.45] and [62.73±3.63] U/L, P<0.01), and increased eNOS activity ([1.16±0.20] vs [3.01±0.47], [2.60±0.26] and [2.32±0.29] U/100 mL, P<0.01).The activity of eNOS was also increased in the salidroside group ([2.32±0.29] U/100 mL, P<0.01).The cell activity in the high-and medium-dose N04 groups was markedly higher than that in the salidroside group (P<0.05), and so was the eNOS activity in the high-dose N04 group and the LDH level in the medium-and low-dose N04 groups (P<0.05).In comparison with the normal control group, the expressions of HIF-1α mRNA, HIF-1α protein and VEGF protein were significantly up-regulated in the hypoxia model group (P<0.01) while that of the pVHL protein markedly down-regulated (P<0.01).Compared with the hypoxia model group, the expressions of HIF-1α mRNA, HIF-1α protein and VEGF protein were remarkably reduced (P<0.05), while that of the pVHL protein markedly elevated (P<0.05).Both the expressions of VEGF mRNA and HIF-1α protein were significantly lower in the medium-and low-dose N04 groups than in the salidroside group (P<0.05).Conclusion N04 can protect vascular endothelial cells against hypoxia-induced injury by regulating the expression of HIF-1α-related factors and eNOS.