The population of patients with congenital heart disease (CHD) is continuously increasing with more and more patients reaching adulthood. A significant portion of these young adults will suffer from arrhythmias due to the underlying congenital heart defect itself or as a sequela of interventional or surgical treatment. The medical community will encounter an increasing challenge as even most of the individuals with complex congenital heart defects nowadays become young adults. Within the past 20 years, management of patients with arrhythmias has gained remarkable progress including pharmacological treatment, catheter ablation, and device therapy. Catheter ablation in patients with CHD has paralleled the advances of this technology in pediatric and adult patients with structurally normal hearts. Growing experience and introduction of new techniques like the 3D mapping systems into clinical practice have been particularly beneficial for this growing population of patients with abnormal cardiac anatomy and physiology. Finally, device therapies allowing maintanence of chronotropic competence and AV conduction, improving haemodynamics by cardiac resynchronization, and preventing sudden death are increasingly used. For pharmacological therapy, ablation procedures, and device therapy decision making requires a deep understanding of the individual pathological anatomy and physiology as well as detailed knowledge on natural history and long-term prognosis of our patients. Composing expert opinions from cardiology and paediatric cardiology as well as from non-invasive and invasive electrophysiology this position paper was designed to state the art in management of young individuals with congenital heart defects and arrhythmias.

The crystal growth of CaTiO(3) hollow crystals with different microstructures has been investigated. In a water-free poly(ethylene glycol) 200 (PEG-200) solution, CaTiO(3) nanocubes formed first. The nanocubes underwent an oriented self-assembly into spherical particles, enhanced by the surface-adsorbed polymer molecules. Since the growth of nanocubes and their aggregation took place simultaneously, the nanocubes in the outer shells were larger than those in the cores. Disappearance of the small nanocubes in the cores of the spheres during an Ostwald ripening process led to spherical hollow crystals. Addition of a small amount of water (1.25 vol %) in the polymer solution enhanced surface recrystallization of the aggregated spheres, forming a cubic morphology. The orthorhombic distortion of the perovskite CaTiO(3) structure did not have a significant effect on the nanocube aggregation, resulting in a domain structure in the shells. Single-crystalline hollow cubes were produced with a slightly higher water content, e.g., 5 vol %. This process of (1) aggregation of nanocubes and (2) surface crystallization followed by (3) surface-to-core extension of recrystallization gives a good example of the reversed crystal growth route in ceramic materials. The proposed formation mechanism of the hollow CaTiO(3) crystals would enable us to control the microstructures of these materials and to explain the formation of many other hollow crystals.

Standard use of cool-tip RFA was dangerous for pancreatic head cancer close to portal vein, in which a 5-mm minimum safe distance between RFA site and major peripancreatic vessels might not be enough to avoid injury to the vessels.

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1. The kinetic properties of cloned mouse embryonic nicotinic acetylcholine receptors (AChRs) expressed in HEK 293 cells or Xenopus oocytes were examined using high concentrations of acetylcholine (ACh), carbamylcholine (CCh), or tetramethylammonium (TMA). The rate constants of agonist binding and channel gating were estimated by fitting kinetic models to idealized open and closed intervals over a range of agonist concentrations. 2. Once doubly liganded, TMA‐activated receptors open at approximately 3000 s‐1. The equilibrium binding constants for TMA are 525 and 12,800 microM. Doubly liganded CCh‐activated receptors open at approximately 11,500 s‐1; the equilibrium binding constants for this agonist are 14 and 570 microM. If we assume that doubly liganded, ACh‐activated receptors open at 60,000 s‐1, then the equilibrium binding constants for ACh are 20 and > 650 microM, similar to those for CCh. For all three agonists the higher affinity site both binds and releases agonists more slowly than does the lower affinity site. 3. ACh and CCh bind to the two sites equally rapidly, at approximately 2 x 10(7) and 4 x 10(7) M‐1 s‐1 at the first and second binding sites, respectively. Compared with ACh, the TMA association rate is approximately 100 times slower at the first binding site, and approximately 30 times slower at the second binding site. These results indicate that at both binding sites the association rate of TMA is not limited by diffusional or steric factors. 4. All three agonists dissociate from the receptor binding sites at similar rates. The dissociation rate for all agonists was approximately 40 times slower at the first binding site than at the second. These results suggest that the interaction of the quarternary amine moiety with the receptor determines the rate of release of the agonist, and that the nature of this interaction is quite different at the two binding sites. 5. Although the channel opening rates for the three agonists varied approximately 20‐fold, the channel closing rates were not strongly agonist dependent, and varied less than 3‐fold. We speculate that the ester moiety of the agonist promotes both rapid binding and fast opening of the ligand receptors, and that interactions of the quarternary amine moiety of the agonist with the receptor determine the channel closing rate constant.

Epidemiological studies have indicated that obesity is associated with colorectal cancer. The obesity hormone leptin is considered as a key mediator for cancer development and progression. The present study aims to investigate regulatory effects of leptin on colorectal carcinoma. The expression of leptin and its receptor Ob-R was examined by immunohistochemistry in 108 Chinese patients with colorectal carcinoma. The results showed that leptin/Ob-R expression was significantly associated with T stage, TNM stage, lymph node metastasis, distant metastasis, differentiation and expression of p-mTOR, p-70S6 kinase, and p-Akt. Furthermore, the effects of leptin on proliferation and apoptosis of HCT-116 colon carcinoma cells were determined. The results showed that leptin could stimulate the proliferation and inhibit the apoptosis of HCT-116 colon cells through the PI3K/Akt/mTOR pathway. Ly294002 (a PI3K inhibitor) and rapamycin (an mTOR inhibitor) could prevent the regulatory effects of leptin on the proliferation and apoptosis of HCT-116 cells via abrogating leptin-mediated PI3K/Akt/mTOR pathway. All these results indicated that leptin could regulate proliferation and apoptosis of colorectal carcinoma through the PI3K/Akt/ mTOR signalling pathway.

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