Image quality evaluation of iterative model reconstruction on low tube voltage (80 kVp) coronary CT angiography in an animal study.

BACKGROUND: Iterative model reconstruction (IMR) is a newer generation iterative reconstruction method, but its value on coronary computed tomography (CT) angiography requires investigation. PURPOSE: To evaluate coronary image quality using IMR at a low-tube voltage of 80 kVp on coronary CT angiography in miniature pigs. MATERIAL AND METHODS: Five healthy miniature pigs underwent prospective electrocardiogram-gated coronary 256-slice CT angiography at 120 kVp and 80 kVp tube voltages, respectively. Filtered back projection (FBP) was used to reconstruct the 120 kVp standard-dose (SD) image sets (SD-FBP group), while iDose(4) and IMR were used to reconstruct the 80 kVp low-dose (LD) image sets (LD-iDose(4) and LD-IMR groups). Objective and subjective image qualities were compared among three groups. RESULTS: There were no significant differences in mean CT values of the ascending aorta, left main coronary artery, and right coronary artery between the LD-IMR and LD-iDose(4) groups (P > 0.05), but the values were significantly lower in the SD-FBP group than in those two groups (P < 0.05). The image noise in the LD-IMR group (21.5 ± 3.9 HU) was significantly lower than in the LD-iDose(4) (63.7 ± 9.8 HU) and SD-FBP (50.6 ± 4.6 HU) groups (P < 0.05). The signal-to-noise and contrast-to-noise ratios were significantly higher in the LD-IMR group than in the LD-iDose(4) and SD-FBP groups, respectively (P < 0.05). Subjective scoring of image noise, streak artifacts, and overall image quality indicated that the LD-IMR group was consistently superior to the LD-iDose(4) and SD-FBP groups (P < 0.05). CONCLUSION: IMR can significantly improve image quality at a low-tube voltage (80 kVp) with a 66% radiation dose reduction on coronary 256-slice CT angiography in miniature pigs.

[Mechanism of Electropuncture for Reducing Diet-induced Obesity Rat Weight through Hypothala- mus TSC1 -mTOR Signal Pathway].

OBJECTIVE: To explore the mechanism of electropuncture (EA) for reducing diet-induced obesity (DIO) rat weight through tuberous sclerosis complex 1 (TSC1 )-mammalian target of rapa- mycin (mTOR) signal pathway in hypothalamus. METHODS: Forty male SD rats were randomly divided into the model group (n =30) and the normal control group (n =10). DIO rat model was prepared by high fat forage for 12 successive weeks. Successfully modeled 19 rats were further randomly divided into the model group (n =9) and the EA group (n =10). EA at Tianshu (ST25) , Sanyinjiao (SP6) , Zhongwan ( RN12) , Zusanli (ST36) was performed in the EA group, 5 successive days per week with a 2-day rest, 4 weeks in total. No intervention was given to rats in the model group and the normal control group. Body weight was observed in all rats. Methylation of TSC1 promotor was detected by bisulfite sequencing method. mRNA expression of mTOR in hypothalamus was detected by RT-PCR. RESULTS: After EA treatment body weight in the EA group were obviously reduced (P <0. 05). Compared with the normal control group, body weight was not statistically different between the model group and the EA group after treatment (P> 0. 05). Methylation rate of TSC1 promotor was higher in model group (94. 0% ±4. 5%) than in the normal control group (87. 0% ±3. 6%) and the EA group (87. 4% ±3. 9%) (P <0. 05). Expression of mTOR in the model group (1. 84 ±0. 51) was higher than that in the normal control group (1. 02 ±0. 22) and the EA group (1. 46 ±0. 29) (P <0. 05). CONCLUSION: EA could lower DIO rats' body weight by down-regulating methylation rate of TSC1 promotor and regulating expression of mTOR in hypothalamus.

[Tsc1 promoter methylation rate, mTOR expression in food-induced obese rat hypothalamus].

OBJECTIVE: To investigate the methylation rate of tuberous sclerosis complex 1 (Tsc1) promoter and expression of mammalian target of rapamycin (mTOR) in food-induced rat hypothalamus. METHODS: 16 male SD rats were divided into high fat diet induced group (8 rats) and normal control group (8 rats) feeding for 12 weeks. Body mass, mass of celiac fat, celiac fat/body mass were measured. Methylation of Tsc1 promoter, mRNA and protein expression of mTOR were detected by bisulfite sequencing method, RT-PCR and Western blot, respectively. RESULTS: Mass of celiac fat, celiac fat/body mass were higher in food-induced rat than that in control group. There were 11 methylation sites in SD rat hypothalamus. Obese group has significantly higher methylation rates (94.50% +/- 4.66%) than that of control group (86.60% +/- 3.49%) (P<0.002). The mRNA and protein expression of mTOR were noted lower in control group than in obese group (P<0.05). CONCLUSION: The increased methylation rate of Tsc1 promoter in food-induced rat hypothalamus and up-regulated expression of mTOR, downstream gene of Tsc1 may promote the obesity.