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BackgroundGenetic factors play a critical role in the onset and progression of obesity. Brown adipose tissue (BAT) activity is also critical for adiposity. The objective of this study was to evaluate the prevalence and effects of gene polymorphisms related to BAT in pediatric obesity.MethodsA case-control study with 270 non-obese and 86 obese children was performed. All participants underwent genotyping of type 2 deiodinase (DIO2) Thr92Ala (rs225014), uncoupling protein 1 (UCP1) -3826 A/G (rs1800592), and β3 adrenergic receptor (β3AR) Trp64Arg (rs4994).ResultsIn the case-control study, the prevalence of the homozygous Ala/Ala allele of the DIO2 gene in the obese group was 15.1 % versus 6.3 % in the non-obese group, resulting in an odds ratio (OR) of 3.393 (95% confidence intervals [CI], 1.498-7.687, P = 0.003). The genotype distribution of UCP1-3826 A/G and ß3AR Trp64Arg did not significantly differ between the obese and the non-obese groups, and the ORs were 1.831 (95% CI, 0.955-3.512, P = 0.069) and 0.819 (95% CI, 0.263-2.555, P = 0.731), respectively.ConclusionsThe results of this study indicate that the homozygous Ala/Ala allele of the DIO2 gene is associated with an increased risk of obesity in children.

To investigate the clinical applicability of the three-dimensional (3D) myocardial imaging using a newly developed system (the Application Visualization System-Medical Viewer), thallium-201 myocardial single photon emission computed tomography was performed in 19 patients with previous myocardial infarction before and after treatment with nisoldipine. We have developed a new method for automatically reconstructing 3D imaging for the stereoscopic evaluation of myocardial perfusion. The left ventricular myocardial volume with a radioisotope countor = 50% of maximum was calculated by using the conventional surface rendering method. With these images, the effect of nisoldipine on myocardial perfusion was assessed and the myocardial volume with a radioisotope countor = 50% of maximum was compared. In fifteen (88%) of 19 patients, myocardial perfusion increased in the infarct areas after nisoldipine treatment. Nisoldipine significantly increased the myocardial volume with a radioisotope countor = 50% of maximum from 141 +/- 17 to 153 +/- 18 ml on the stress 3D imagings. These findings indicate that nisoldipine improved myocardial perfusion during exercise. 3D imaging provided stereoscopic assessment of the changes in myocardial perfusion following treatment with nisoldipine and also detected transient enlargement of the left ventricular lumen induced by exercise.

Because endoscopic examinations are a crucial first step in the diagnosis of carcinomas, we have analyzed point mutations of the c-K-ras and p53 genes using biopsied samples. There is no previous report of such an approach, using only biopsied materials. We analyzed point mutations of the c-K-ras and p53 genes using 60 colorectal and 31 gastric tumor biopsy specimens. None of the gastric and seven of the colorectal tumors had mutations of the c-K-ras gene. p53 gene mutations were detected in six gastric carcinomas [two out of 11 intramucosal carcinomas (18.2%) and four out of 11 invasive carcinomas (36.4%)]. Eight of 15 invasive colorectal carcinomas (53.3%) showed point mutations in the p53 gene. Although point mutation frequencies in this study were relatively low when compared with previous reports in which surgical samples were used, our study shows that biopsied specimens are adequate and useful for analysis of gene point mutations.

The effect of nicorandil on myocardial perfusion in ischaemic heart disease has been studied using exercise-load Tl-201 myocardial SPECT (Ex-SPECT). Ex-SPECT was carried out in 12 patients with previous myocardial infarction (OMI) and 9 with angina pectoris (AP) before and after administration of nicorandil 15 mg/day, for three or more weeks; % Tl uptake and the washout rate in infarcted or ischaemic areas were calculated from short axial images using the Bull's eye method.

To evaluate sympathetic dysfunction of the heart, one of the factors responsible for heart failure in patients with dilated cardiomyopathy (DCM), we performed 123 I-metaiodobenzylguanidine ( 123 I-MIBG) myocardial single photon emission tomography (SPET) in 22 cases of DCM. There were significant relationships between severity scores and defect scores for the early and delayed images. When the data acquired by 123 I-MIBG myocardial SPET were compared with left ventricular function, the extent score (r = -0.754, P < 0.01) and severity score (r = -0.693, P < 0.01) for the early images were both significantly correlated with left ventricular ejection fraction (LVEF). For the delayed images also, a good correlation was obtained between LVEF and extent score (r = -0.704, P < 0.01) and between LVEF and severity score (r = -0.801, P < 0.01). The washout rate for the entire left ventricle, calculated from the early and delayed images, also correlated with LVEF (r =-0.643, P < 0.01). Since the 123 I-MIBG defect on the early images was shown to be significantly related to left ventricular function, a decrease in neuronal uptake at sympathetic nerve endings appears in the main to account for the 123 I-MIBG defect on the early images. The regional washout rate was increased compared to that in the control group (P < 0.01). It was particularly high in the inferior wall, suggesting that acceleration of turnover and poor retention in the area of the 123 I-MMBG defect on the early images and then the entire left ventricle was strongly associated with the 123 I-MIBG defect on the delayed images. Our results suggest that 123 I-MIBG myocardial SPET may be useful in determining the severity of DCM.

Left ventricular myocardial disorders due to volume overload were investigated by TI-201 myocardial SPECT (TI-201 SPECT) in patients with aortic or mitral regurgitation, and its utility for timing cardiac valve replacement was studied. There were significant correlations between TI-201 scores and electrocardiographic changes and the New York Heart Association classification. There also were favorable correlations between TI-201 scores and the left ventricular end-diastolic dimension and between TI-201 scores and left ventricular ejection fraction, and a close relationship between the presence of a left ventricular myocardial disorder and left ventricular diameter. These results suggest that myocardial perfusion abnormalities and left ventricular myocardial disorders may accompany left ventricular dilatation owing to volume overload. After valve replacement, left ventricular end-diastolic dimension normalized, and TI-201 scores improved slightly, suggesting normalization of myocardial perfusion. When moderate or more severe TI-201 defects are present on TI-201 SPECT images, in addition to inverted TI-201 waves on the electrocardiogram or a left ventricular end-diastolic dimension of 65 mm or more, cardiac valve replacement should be considered.

The development of gap junctions in the human gastric mucosa has been examined to see if there is any relation to gastric ulcer. Freeze fracture replicas were prepared from the endoscopic biopsy specimens of 20 patients with gastric ulcer (15 men and five women, aged 49 (13) years) and seven healthy volunteers (four men and three women, aged 41 (19) years). Large fractured areas of lateral cell membranes of surface mucous cells were observed randomly at a direct magnification of 15,000 using electron microscopy. Small gap junctions were observed between gastric surface mucous cells in all healthy volunteers. Gap junctions in the patients with gastric ulcer were significantly fewer than in the healthy volunteers. In addition, gap junctions in patients with recurrent ulcer were significantly fewer than in those with first onset ulcer. There was no obvious relationship between age and the development of gap junctions in patients with gastric ulcer or in healthy volunteers. In areas of intestinal metaplasia, gap junctions were occasionally seen between absorptive cells of the villi, but not in the lateral membranes of goblet cells. These findings suggest that loss of intercellular communication via gap junctions is associated with gastric ulcer formation.