The expression of serum and glucocorticoid-induced protein kinase in the renal cortex of diabetic rats was examined, and the function of signal transduction mediated by SGK1 in diabetic nephropathy and its modulatiqn by fluvastatin were also investigated. 24 male Wistar rats were randomly divided into normal control group (n = 8), diabetic nephropathy group (n = 8) and fluvastatin-treated diabetic nephropathy group (15 mg/kg/d, n = 8). The metabolic parameters were measured at the 8th week. The expression of transforming growth factor beta1 (TGF-beta1) and fibronectin (FN) was immunohistochemically examined. The expression of SGK1 was detected by RT-PCR and Western blot, and CTGF mRNA was assessed by RT-PCR. As compared to DN, blood glucose, 24-h urinary protein, Cer and kidney weight index were all decreased and the weight was increased obviously in group F. At the same time, mesangial cells and extracellular matrix proliferation were relieved significantly. The levels of cortex SGK1 mRNA and protein were up-regulated, and both TGF-beta1 and FN were down-regulated by fluvastatin. The mRNA of SGK1 was positively correlated with the CTGF, TGF-beta1 and FN. SGK1 expression is markedly up-regulated in the renal cortex of DN group and plays an important role in the development and progress of diabetic nephropathy by means of signal transduction. Fluvastatin suppressed the increased SGK1mRNA expression in renal cortex and postponed the development of diabetic nephropathy.

AIM: Eight melanoma cell lines were establi sh ed from human melanoma specimen and designated as HME 1-HME 8, and their charact eristics of cell biology and immunology in vitro were studied. METHODS: The tissues from biopsies of human melanoma were cultur ed in RPMI 1640 media. After growing to 90% confluence, the cells were detached for subculture and then their characteristics, including morphology, growth kine tic, tumor antigen and tumorigencity in nude mice were studied. RESULTS: These cell lines have been passaged more than 100 times within 2 years. Their characteristics demonstrated: ① The population doubling time calculated in the log phase of growth were 34.2-59.5 h. ② The cloning ef ficiency in soft agar averaged 8.6%-26.2%. ③ The melanoma cells transplan t ed in nude mice were high tumorigencity. ④ Karyo-type analysis showed that aneu ploidy with the modal chromosomal number 64-117. ⑤ Rich ribosomes and melanoid grains in the cytoplasm were observed under electronic microscope. ⑥ Immunohist ochemistry analysis showed that there were a lot of brown grains in the cytoplas m. ⑦ Detection of tumor-antigen demonstrated that melan-A antigen was 75.0%, M AGE-1 was 50.0%, MAGE-2 was 37.5%, MAGE-3 was 62.5%, respectively, for eight melanoma cell lines. CONCLUSION: The melanoma cells have immortalized after being cul tured in vitro and has specific characteristics of malignant melanoma.

Objective To investigate the frequency of lesions detection in patients with cerebral infarction (CI) with SPECT/CT. To investigate fluctuation of regional cerebral blood flow (rCBF) and its relationship with clinical symptoms. Methods Sixty-seven CI patients without cerebellar lesion were randomly selected. The rCBF in the regions of interest (ROI) was examined by SPECT/CT, which was collected from the frontal lobe, temporal lobe, parietal lobe, occipital lobe, thalamus, basal ganglia and cerebellum. The rCBF index was calculated. The association between fluctuation of rCBF index and clinical symptoms of patients was explored. Results There were 251 positive regions in all viewing regions , the total positive rate was 31.2%. The left side was 38.1%, while the right side was 24.4% (χ2=17.522,P < 0.01). In normal group, there were no statistical difference of average rCBF between two halves (P > 0.05). However, the average rCBF on the left parietal lobe was lower (P < 0.01). The average rCBF in the abnormal group was lower than that in ipsilateral normal group (P < 0.01). The average rCBF index in the abnormal group was higher (P < 0.01). In normal group , the average rCBF on the frontal lobe and parietal lobe was low , but the average rCBF on the thalamus and basal ganglia was high (P < 0.01). In abnormal group, there were no statistical difference in the average rCBF (P >0.05). rCBF≥0.7 is a clinical sign of abnormal ROI. Conclusion 30% of ROI of CI patients have lesions and the positive rate of the left side was higher. The biological rCBF values of all lobes were different. Therefore, rCBF index could be used to reflect whether the ROI is normal. rCBF≥0.7 could be used as a sign to quantitatively assess abnormal ROI in clinical practice.

The expression of serum and glucocorticoid-induced protein kinase in the renal cortex of diabetic rats was examined, and the function of signal transduction mediated by SGK1 in diabetic nephropathy and its modulation by fluvastatin were also investigated. 24 male Wistar rats were randomly divided into normal control group (n = 8), diabetic nephropathy group (n= 8) and fluvastatin-treated diabetic nephropathy group(15 mg/kg/d, n=8). The metabolic parameters were measured at the 8th week. The expression of transforming growth factor β1 (TGF-β1 ) and fibronectin (FN) was immunohistochemically examined. The expression of SGK1 was detected by RT-PCR and Western blot, and CTGF mRNA was assessed by RT-PCR. As compared to DN, blood glucose,24-h urinary protein, Cer and kidney weight index were all decreased and the weight was increased obviously in group F. At the same time, mesangial cells and extracellular matrix proliferation were relieved significantly. The levels of cortex SGK1 mRNA and protein were up-regulated, and both TGF-β1 and FN were down-regulated by fluvastatin. The mRNA of SGK1 was positively correlated with the CTGF, TGF-β1 and FN. SGK1 expression is markedly up-regulated in the renal cortex of DN group and plays an important role in the development and progress of diabetic nephropathy by means of signal transduction. Fluvastatin suppressed the increased SGK1mRNA expression in renal cortex and postponed the development of diabetic nephropathy.

Thyroid cancer is one of the common malignant tumors in the endocrine system, and its incidence is increasing year by year. At present, the main diagnostic methods for thyroid cancer are ultrasound and thyroid puncture cytology. However, due to low sensitivity and/or specificity, it is increasingly difficult to meet the current clinical diagnostic needs. The discovery of biomarkers in thyroid cancer provides important clues for the diagnosis, pathogenesis and prognosis of the disease. As one of the essential trace elements in human body, iodine is closely related to the thyroid gland. Clarifying the relationship between iodine nutritional status and biomarkers of thyroid cancer has important practical significance for the diagnosis, pathogenesis and prognosis of thyroid cancer. Based on the research of systems biology, this article analyzes the influence of iodine nutritional status on biomarkers of thyroid cancer from four aspects of gene, transcription, protein and metabolism,

Objective: To investigate the molecular characterization of adult diarrhea cases caused by enterotoxic Escherichia coli (ETEC) and explore the practical model of epidemiology for laboratory technique and data needs based on the surveillance network. Methods: Epidemiological design and sampling targeted adult cases ETEC caused diarrhea in epidemic season. The enterotoxin type, serogroup, resistance, colonization factor and molecular type of ETEC were identified. Multiple dynamic phenotypic characteristics of ETEC were indicated by multidimensional and multivariable data. Results: From 2016 to 2018, 84 eligible ETEC strains were detected. The dominant serums/toxins were O∶6 (STh), O∶25 (LT), O∶159 (STh), O∶153 (STh). O∶6 (STh+CS21), which replaced O∶25 and O∶159 as the popular clones in 2018. Six cases of O∶153 (STh+CFA/I+CS8+PT34) in outbreak in 2017 were imported ones. The resistance rates of ETEC strains detected in adults to sulfasoxazole, naproxinic acid, ampicillin and azithromycin were more than 30%, multidrug resistance (MDR) reached 58.3%. Serum/toxin types suggested that attenuated strains were more likely to become MDR. Molecular typing confirmed that the genetic similarity of the dominant clone of O∶6 serogroup (PT20-24) was higher than O∶25 and O∶159. There was a high correlation between the minimal inhibitory concentration (MIC) of azithromycin and the resistant gene mphA (87.5%, 28/32). O∶6 (STh+CS21+mphA) resistant clone was first detected in 2016. Conclusion A new epidemic clone in adult ETEC diarrhea cases in Shanghai was O∶6 (STh+CS21+mphA). For the first time the association between azithromycin resistance gene mphA and a serum group of ETEC was observed. Multidimensional and multivariate analysis techniques based on epidemiology can help reveal the potential transmission pattern of ETEC for the accurate surveillance and early warning of outbreaks.