ObjectiveTo derive and evaluate the formula of exactly calculating the contrast dosage used during pulmonary CT angiography ( CTPA ). Methods Time density curves in 27 patients who underwent CTPA were collected and analyzed,the formula for calculating contrast dosage during CTPA was derived.68 patients suspected of pulmonary embolism ( PE ) clinically but no PE on CTPA were divided randomly into group A,with bolus tracing technique ( n =26 ),and group B,with small dose injection contrast test (SDCT) (n =42).The CT values of the right main pulmonary artery (RMPA),right upper pulmonary vein ( RUPV),right posterior basal PA,right lower PV (RLPV) and the aorta were calculated.The total contrast dosage and the hard beam artifact in the SVC were compared between the two groups.Student's t test,Chi-square test and Mann-Whitney U test were used.ResultsThe ratio of the time from starting injection to enhancement peak of caudal end of SVC and the time to enhancement peak of the main pulmonary trunk was 0.65 ±0.09 (about 2/3),the formula for contrast dosage calculation was derived as (DTs/3 + STs/2) FR ml/s.The CT values of RMPA and RLPA between the two groups[ (301 ±117),(329 ± 122) and (283 ±95),(277 ±98) HU respectively] were not significantly different (t =1.060,P =0.292 ;t =2.056,P =0.044),but the differences of CT values in the paired PA and PV between the two groups (median were 22.5,58.0 and 170.5,166.5 HU respectively ) were significant (U =292,P =0.001 and U =325,P =0.005),contrast artifact of the SVC (grade 1-3) in group B ( n =34,7,1 respectively) was significantly less than in group A (n =11,10,5 respectively,x2 =10.714,P =0.002),the contrast dosage injected in group A was ( 87.6 ± 7.3 ) ml,and in group B was ( 40.0 ±5.4) ml (P ＜0.01 ).ConclusionCTPA with SDCT technique is superior to that with conventional bolus tracing technique regarding contrast dosage and contrast artifact in the SVC.

Objective To study the CT manifestations of delayed traumatic hematomas of the brain and evaluate their diagnostic significance in predicting the delayed traumatic brain hematoma. Methods The manifestations of initial CT studies and follow-up CT examinations of 31 delayed traumatic brain hematomas were analyzed. Another 50 CT studies of head trauma without delayed brain hematomas were included randomly as control. Results The abnormal findings of CT studies of the 31 delayed traumatic brain hematomas included: (1)Decreased density of the local brain parenchyma and disappeared difference between gray and white matter of the same area in 18 cases; (2)Local subarachnoid space hemorrhage in 24 cases; (3)Slight mass effect of local brain parenchyma in 16 cases. (4)Subdural hematoma in 9 cases. The locations of the abnormalities were roughly the same with the delayed hematoma except one local subarachnoid space hemorrhage, which was in the opposite of the delayed hematoma. The appearing rate of those abnormal findings in the control group was low and the difference was statistically significant. Conclusion The decrease of density of local brain parenchyma, the disappeared difference between the gray and white matter, local subarachnoid space hemorrhage, and local swollen of brain presented in the initial CT study of the patient with head trauma should be taken as indicators of delayed hemorrhage of the same area of brain, and it is necessary to do follow-up CT studies to exclude it.

BACKGROUND: Insulin like growth factor 2 (IGF2) is an important embryonic mitosis growth promoting factor, whichplays a critical role in the process of maintaining normal cell growth. The gene expression of IGF2 is under epigeneticregulation in the way of genomic imprinting. Imprinting loss of IGF2 is likely to be associated with the abnormaldevelopment of the individual and tumorigenesis.OBJECTIVE: To investigate the effect of imprinting loss of IGF2 gene on the differentiation of mouse embryonic stemcells into islet-like cells.METHODS: Two kinds of mouse embryonic stem cells (SF1-G and SF1-1) were induced to differentiate into islet-likecells in vitro. The expression of Insulin gene was detected by real-time PCR and cell immunofluorescence. Theexpression of IGF2 was detected by the polymerase chain reaction-restriction fragment length polymorphism in the cellsbefore and after induced differentiation. The level of insulin released at terminal differentiation stage was tested by insulinrelease assay in vitro.RESULTS AND CONCLUSION: (1) There was no change in the imprinting state of the two kinds of mouse embryonicstem cells with normal and imprinted IGF-2 gene before and after differentiation. (2) In the induced cells, the expressionlevel of insulin in the SF1-1 group was higher than that in the SF1-G group, although there was no significant differencein the insulin release between the two kinds of cells. (3)The imprinting loss of IGF-2 gene may be related to theup-regulation of insulin mRNA expression in terminal cells during induced differentiation.

Objective To investigate the molecular regulatory mechanism of glucagon like peptide 1 (GLP-1) on proliferation, differentiation and apoptosis of human umbilical cord blood endothelial progenitor cells (EPCs). Methods EPCs were isolated from the umbilical cord blood of healthy pregnant women and cultured in 6-hole cell plate at 2×105 density in vitro, transfected with empty vector plasmid (control group), pcDNA3-GLP-1 plasmid (GLP-1 group), pcDNA3-GLP-1plasmid+AMD3100 (GLP-1+AMD3100 group) and simple AMD3100 (AMD3100 group). The pcDNA3-GLP-1 was transfected into EPCs. The 25μmol/L AMD3100 was used to block the SDF-1/CXCR4 signal pathway of EPCs for 1 h. The cell proliferation was determined by MTT method. The mRNA expressions of differentiation and apoptosis related genes PPARγ, C/EBPα and Caspase-3 were investigated by RT-PCR, and Caspase-3 activity was determined by Caspase-3 activity assay kit. Results Compared to control group, AMD3100 inhibitor showed no effects on cell proliferation, differentiation and apoptosis, while over-expression of GLP-1 in EPCs obviously promoted cell proliferation, and differentiation related genes PPARγand C/EBPαmRNA expression, but down-regulated mRNA expression and the activity of Caspase-3 significantly (P＜0.05), indicating that GLP-1 increased proliferation and differentiation of EPCs while decreased cell apoptosis. When the SDF-1/CXCR4 signaling pathway was blocked by AMD3100, over-expression of GLP-1 induced promotion of cell proliferation, and the differentiation was decreased significantly and the apoptosis was significantly increased (P＜0.05). Conclusion These data confirm that GLP-1 might promote EPCs proliferation and differentiation, and inhibit cell apoptosis through the regulation of the SDF-1/CXCR4 signaling pathway.

Objective To observe the effects of insulin-like growth factor-2 (IGF2) in the course of mouse embryon-ic stem cells induced to differentiate into islet-like cells. Methods Mouse ES cells were induced to differentiate into islet-like cells in vitro. The expression of islet specific markers was tested by RT-PCR and immunofluorescence assay. RT-PCR/RFLP was used to test the imprinted genes IGF2 parental expression in cells at different stages. Results Islet specific mark-ers were expressed in differentiated cells, such as insulin, glucagon and C-peptide. PCR-RFLP showed that imprinted genes IGF2 derived from embryonic stem cells were biallelic expression and loss of imprinting. Conclusion Gene imprinting sta-tus of IGF2 was changed in differentiated cells in vitro.

Aim To investigate the relationship be-tween the cardioprotection of apigenin ( Api ) from an-oxia/reoxygenation ( A/R) injury and Bcl-2 pathway. Methods H9 c2 cardiomyocytes were cultured and di-vided into normal control group, A/R group, Api pre-treatment group ( Api ) , Api + Bcl-2 inhibitor group ( Api + ABT-737 ) . Expression of Bcl-2 was deter-mined by Western blot,and cell viability was measured by MTT method. LDH, SOD, GSH-Px, MDA activity were determined by chromometry. ROS generation, mi-tochondrial membrane potential and apoptosis were de-termined by flow cytometry. Results 25h after apige-nin precondition,the expression of Bcl-2 was upregulat-ed in cardiomyocytes ( P <0. 01 ) . In the group pre-treated with 40 μmol · L-1 apigenin before A/R, the activity of LDH in culture medium decreased; the ac-tivity of intracellular SOD, GSH-Px increased; the content of MDA and ROS generation decreased; cell viability increased; mitochondrial membrane potential could be more stable and cell apoptosis decreased ( P<0. 01 ) . However, all these protective effects were attenuated significantly in the group pretreated with apigenin and Bcl-2 inhibitor ABT-737 . Conclusion The effect of apigenin against A/R injury in cardiomyo-cytes involves Bcl-2 pathway, and at least partly de-pends on its effect on upregulating the expression of Bcl-2 .

Objective To summarize the cl inical characteristics and imaging features of psittacosis. Methods The clinical features and imaging appearances of 3 cases with acute psittacosis were retrospectively analyzed. The related literature was reviewed . Results The clinical manifestation of psittacosis was high fever in the patients. Physical findings included pulse-temperature dis sociation, localized lung crackles, hepatomegaly, and splenomegaly. Laboratory findings showed elevation of ESR in all cases, and liver dysfunction was present in 2 cases. The counts of white blood cells were normal, but the percent of ne utrophils might be increased. The chest X-ray and CT scan showed air-space co nsolidation and ground-glass attenuation in the lung, and miliary, nodular, or consolidated shadows were found in pathological areas. Pleural effusions were a lso present in 2 cases. Psittacosis was diagnosed from the history of exposure to infected parrots and elevation of the IgG and IgM titer for Chlamydia psittac i. Erythromycin was effective in all 3 patients. Conclusion Although the appearance of psittacosis on clinical findings and chest X-r ay and CT scan is not characteristic, psittacosis can be diagnosed with the comb ination of the history of exposure to infected parrots and laboratory findings. CT scan can reveal the focus earlier and accurately, and catching the imaging f eatures of psittacosis is helpful in differential diagnosis.

Objective:To investigate the effects of hyperuricemia on the prognosis of IgA nephropathy (IgAN) using propensity score matching (PSM) method.Methods:IgAN patients proven by biopsy were included. PSM was used to match patients. Kaplan-Meier method was used for survival analysis, and Cox regression analysis was used to analyze the effects of hyperuricemia on IgAN prognosis. Primary outcome events were defined as death, or end-stage renal disease (dialysis, transplantation), or a decrease in estimated glomerular filtration rate (eGFR) greater than 40%. Renal outcome was defined as end-stage renal disease (dialysis, transplantation), or a decrease in eGFR greater than 40%.Results:A total of 1 454 IgAN patients were included in this study, including 850 females and 604 males. Uric acid level was (368.26±92.87) μmol/L in the males, and (277.23±92.71) μmol/L in the females. The median follow-up time was 85.00(56.10, 106.33) months. During the follow-up period, a total of 134 patients reached the primary outcome events, including 5 deaths, 24 dialysis patients, 5 kidney transplant patients, and 100 patients with eGFR decreased by more than 40%. After 1∶1 matching, 131 males and 159 females in the hyperuricemia group were successfully matched with 131 males and 159 females in the normal uric acid group, and there was no significant statistical difference in each parameter in baseline between the hyperuricemia group and normal uric acid group after matching. Kaplan-Meier survival analysis showed that either before or after matching, the incidence of primary outcome events in male or female patients with hyperuricemia was higher than those with normal uric acid, but there was no statistically significant difference in incidence of primary outcome events between female hyperuricemia group and female normal uric acid group after matching (Log-rank test, χ2=3.586, P=0.058). Cox proportional hazard regression model showed that, in the pre-match fully adjusted model, the hazard ratio ( HR) of entering primary outcome events was 2.29-fold (95% CI 1.27-4.11, P=0.006) for men with hyperuricemia and 1.85-fold (95% CI 1.01-3.37, P=0.045) for women with hyperuricemia compared with those with normal uric acid. In the post-match fully adjusted model, the HR of entering primary outcome events was 2.41-fold (95% CI 1.18-4.93, P=0.016) for men with hyperuricemia and 1.83-fold (95% CI 0.91-3.67, P=0.091) for women with hyperuricemia compared with those with normal uric acid. In the pre-match fully adjusted model, the HR of entering renal outcome events was 2.68-fold (95% CI 1.47-4.88, P=0.001) for men with hyperuricemia and 1.81-fold (95% CI 0.99-3.33, P=0.056) for women with hyperuricemia compared with those with normal uric acid. In the post-match fully adjusted model, the HR of entering renal outcome events was 2.89-fold (95% CI 1.36-6.15, P=0.006) for men with hyperuricemia and 1.81-fold (95% CI 0.88-3.72, P=0.106) for women with hyperuricemia compared with those with normal uric acid. Conclusion:Hyperuricemia may be associated with IgAN progression, and it has a more significant effect on male IgAN patients.

Objective: To analyze the risk factors for large renal hematoma caused by percutaneous renal biopsy (PRB) in order to provide evidence for early clinical prevention and Effective nursing. Methods: The data of 707 patients who underwent PRB in nephrology department in Hangzhou Hospital of Traditional Chinese Medicine from January 2016 to January 2017 were retrospectively identified. Demographic and clinical data were collected, including general status (gender, age, body mass index, histological diagnosis, associated diseases), laboratory indexes and related examination during PRB (serum creatinine, estimated glomerular filtration rate, creatinineclearance rate, serumuricacid, serumalbumin, hemoglobin, platelet count, prothrombin time, activated partial thromboplastin time, kidney size), blood pressure(history of hypertension, systolic blood pressure, diastolic blood pressure and mean arterial blood pressure before PRB). Univariable logistic regression analysis, linear diagnosis, factor analysis, multivariable logistic regression analysis and receiver operating characteristic curve (ROC curve) were used to assess risk factors. Results: Over the period, 707 native kidney biopsies were performed. Hematoma occurred in 609 biopsies (86.1%), including 558 minorhematomacases (78.9%), 51 largehematoma cases (7.2%), no severe complications were observed. Univariable logistic regression analysis of risk factors in 51 patients with large hematoma after PRB found that there were significant differences in renal tubulointerstitial fibrosis, crescents > 25%, serum creatinine, history of hypertension, systolic blood pressure, diastolic blood pressure and mean arterial pressure before PRB (P< 0.05). Compared with the non-hematoma/minor-hematoma group, the blood pressure before PRB increased significantly in large hematoma group (OR=1.414, 95%CI=1.007-1.985, P=0.045) . More patients with a history of hypertension in large hematoma group (OR=1.997, 95% CI=0.995-4.009, P=0.052) .The area under the ROC curve for predicting large hematoma after PRB was 0.634 for blood pressure before PRB and history of hypertension, the Youden index was 0.27. The blood pressure before PRB and hypertension history were used to predict the formation of large hematoma separately, and the Youden index was 0.28 vs. 0.22 (P> 0. 05). Conclusions History of hypertension and blood pressure before PRB were independent risk factors for large renal hematoma after PRB.Patients with history of hypertension were more likely to develop large hematoma than those with no history of hypertension, and those with higher blood pressure before PRB were more likely to develop large hematoma. The history of hypertension and the blood pressure before PRB have certain effect in predicting the formation of large hematoma after PRB. Each of them have a certain predictive effect on the formation of largehematoma after PRB, and the prediction effect trend of blood pressure before PRB is slightly better than that of history of hypertension.