5-Aminolevulinic acid (ALA)-mediated photodynamic therapy (PDT) (ALA-PDT) is a highly selective treatment for malignant cells. ALA-PDT has the potential to develop into a novel therapeutic strategy for various types of cancer. Recently, light-emitting diodes (LEDs), which are inexpensive, stable and easier to handle compared to lasers, have been used in PDT as a light source. However, in colorectal cancer (CRC), the efficacy of ALA-PDT in combination with LEDs has not been fully assessed. Therefore, in this study, we evaluated the antitumor effect of ALA-PDT using various LEDs in colon cancer cells. The HT-29 human colon cancer cell line was used both in vitro and in vivo. HT-29 cells were seeded in 96-well plates. Following 5-ALA administration, cells were irradiated using LEDs at different wavelengths. Three types of LEDs, blue (peak wavelength, 456 nm), white (broad-band) and red (635 nm) were used. Twenty-four hours after irradiation, the cytotoxic effects of ALA-PDT were measured using the 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay. In order to evaluate the antitumor effect of ALA-PDT in vivo, nude mice were inoculated with HT-29 cells. Xenograft mice were injected intraperitoneally with 5-ALA and irradiated with 3 types of LEDs at a measured fluence rate of 96 mW/cm2 and fluence of 32 J/cm2. Each group comprised 6 mice. ALA-PDT was repeated 3 times at weekly intervals. Tumor weights were measured. Compared to the controls, ALA-PDT using LEDs showed significant antitumor effects in vitro and in vivo. The blue and white LEDs demonstrated greater antitumor effects compared to the red LEDs in vitro and in vivo. In particular, tumor inhibition rates in the blue and white LED groups were approximately 88% to those of the control group in the mouse models. In conclusion, ALA-PDT using LEDs is effective and useful in the treatment of CRC cells. This method could be a novel treatment modality for CRC.

Regulation of connexin43 (Cx43) expression affects cell proliferation, differentiation and apoptosis in a gap junctional intercellular communication (GJIC)-independent manner. However, the underlying mechanisms of Cx43-mediated cell cycle suppression are still poorly understood. To elucidate the molecular mechanism of Cx43-mediated cell cycle suppression, we searched for Cx43 interacting proteins by using a proteomics approach. Here, we have identified a Cx43-interacting protein, heat shock cognate protein 70 (Hsc70). We confirmed that Hsc70 directly binds to the C-terminus of Cx43, whereas Hsc54, a splice variant of Hsc70, does not, that Cx43 competes with cyclin D1 for binding to Hsc70, and that the nuclear accumulation of cyclin D1 is reduced by overexpression of Cx43 in a GJIC-independent manner, which is restored by co-overexpression with Hsc70. As a result, the cell proliferation is regulated by Cx43. Our results suggest that Cx43-Hsc70 interaction probably plays a critical role during G1/S progression.

Torsion of the vermiform appendix is a rare disorder, which causes abdominal symptoms indistinguishable from acute appendicitis. We report a case (a 34-year-old male) of secondary torsion of the vermiform appendix with mucinous cystadenoma. This case was characterized by mild inflammatory responses, pentazocine-resistant abdominal pain, and appendiceal tumor, which was not enhanced by the contrast medium on computed tomography presumably because of reduced blood flow by the torsion. These findings may be helpful for the preoperative diagnosis of secondary appendiceal torsion.

Proliferation of pancreatic β-cells is an important mechanism underlying β-cell mass adaptation to metabolic demands. Increasing β-cell mass by regeneration may ameliorate or correct both type 1 and type 2 diabetes, which both result from inadequate production of insulin by β-cells of the pancreatic islet. Transforming growth factor β (TGF-β) signaling is essential for fetal development and growth of pancreatic islets. In this study, we exposed HIT-T15, a clonal pancreatic β-cell line, to TGF-β signaling. We found that inhibition of TGF-β signaling promotes proliferation of the cells significantly, while TGF-β signaling stimulation inhibits proliferation of the cells remarkably. We confirmed that this proliferative regulation by TGF-β signaling is due to the changed expression of the cell cycle regulator p27. Furthermore, we demonstrated that there is no observed effect on transcriptional activity of p27 by TGF-β signaling. Our data show that TGF-β signaling mediates the cell-cycle progression of pancreatic β-cells by regulating the nuclear localization of CDK inhibitor, p27. Inhibition of TGF-β signaling reduces the nuclear accumulation of p27, and as a result this inhibition promotes proliferation of β-cells.

LAC improved short-term outcomes even in very elderly patients.