Evaluation of cephalometric characteristics and skeletal maturation of the cervical vertebrae and hand-wrist in girls with central precocious puberty.

OBJECTIVE: This study aimed to evaluate the differences in cephalometric characteristics and skeletal maturation in girls with central precocious puberty (CPP) via lateral and hand-wrist radiographs. We also aimed to identify the indicators that are most effective for determining skeletal maturity in these patients. METHODS: The study included 70 Korean girls (mean age, 8.5 ± 0.5 years) diagnosed with CPP at the Department of Pediatrics, and 48 normal healthy age-matched girls who visited the Department of Orthodontics and had no history of hormone treatment or growth problems. Skeletal maturation was evaluated using lateral cephalometric and hand-wrist radiographs using cervical vertebrae maturation indicators (CVMI) and skeletal maturity indicators (SMI). RESULTS: The mean mandibular plane angle was smaller in the CPP group than in the control group (35.8° ± 4.9° vs. 39.0° ± 6.5°), resulting in greater posterior facial height (p = 0.003). SMI was significantly greater in the CPP group (3.5 ± 1.4 vs. 2.0 ± 1.0) than in the control group (p = 0.001) and was significantly associated with CPP (r = 0.492; p = 0.001), whereas CVMI was not. CONCLUSIONS: In comparison with the control group, the CPP group exhibited a smaller mandibular plane angle, greater posterior facial height, and greater skeletal maturation. SMI may be more suitable than CVMI for determining skeletal maturation in CPP. Hand-wrist radiography is recommended in addition to lateral cephalogram for predicting growth in girls with CPP.

Maximum intensity projection using bidirectional compositing with block skipping.

BACKGROUND: Maximum intensity projection (MIP) is a volume rendering technique that determines the pixel intensity as the maximum of all values sampled along the viewing direction. MIP has been successfully applied to diagnose bone fractures in computed tomography (CT) and the stenosis of vascular structures in magnetic resonance angiography (MRA). However, MIP has a major drawback in that the depth and occlusion information cannot be perceived in the output images. The most universal way to alleviate this problem is to occasionally change the viewpoint for depth perception. To support this function in real time, MIP should be performed at an interactive frame rate. OBJECTIVE: We develop an efficient rendering algorithm for MIP so that MIP is performed at an interactive frame rate without a loss of image quality. METHODS: The proposed method predicts the position of the maximum intensity for each ray using blockwise maximum bounds, after which it performs bidirectional compositing toward both ends of the ray from this predicted position. During the compositing process, block skipping is used as an acceleration method. RESULTS: The proposed method outperformed the block skipping method using the sequential compositing with a speed-up factor of 2.2 ∼ 2.8 depending on the data set without any degradation of the image quality. CONCLUSION: We proposed an efficient rendering technique for MIP. Our method was superior to the conventional block skipping method with respect to the rendering speed and degree of performance consistency.

Bcl-XL prevents serum deprivation-induced oxidative stress mediated by Romo1.

B-cell lymphoma-extra large (Bcl-XL) has been known to suppress serum deprivation-induced cell death, while reactive oxygen species modulator 1 (Romo1) is responsible for a serum deprivation-induced increase in reactive oxygen species (ROS). Therefore, we investigated whether Bcl-XL expression could inhibit the serum deprivation-induced increase in ROS and cell death, which are mediated by Romo1. We found that Bcl-XL expression effectively blocked serum deprivation- and Romo1-triggered ROS generation. Bcl-XL also inhibited apoptotic cell death induced by both serum deprivation and oxidative stress. From these results, we suggest that increased Bcl-XL expression, which is observed in many cancer cells, confers resistance to oxidative stress in the cancer cells by suppressing Romo1-mediated oxidative stress.

Mitochondrial reactive oxygen species originating from Romo1 exert an important role in normal cell cycle progression by regulating p27(Kip1) expression.

Reactive oxygen species (ROS) steady-state levels are required for entry into the S phase of the cell cycle in normal cells, as well as in tumour cells. However, the contribution of mitochondrial ROS to normal cell proliferation has not been well investigated thus far. A previous report showed that Romo1 was responsible for the high ROS levels in tumour cells. Here, we show that endogenous ROS generated by Romo1 are indispensable for cell cycle transition from G1 to S phase in normal WI-38 human lung fibroblasts. The ROS level in these cells was down-regulated by Romo1 knockdown, resulting in cell cycle arrest in the G1 phase. This arrest was associated with an increase in the level of p27(Kip1). These results demonstrate that mitochondrial ROS generated by Romo1 expression is required for normal cell proliferation and it is suggested that Romo1 plays an important role in redox signalling during normal cell proliferation.