Introduction: Although fentanyl patch (FP) are often used to treat cancer pain because of the low incidence of adverse effects of this formulation, there are cases in which it is impossible to eliminate the pain despite increasing the doses. We report a patient of advanced gastric cancer with abdominal pain, in whom successful pain control was achieved by opioid rotation from FP to continuous intravenous infusion of morphine hydrochloride. Case Report: The patient was a male in his 60's who had been diagnosed as having primary gastric cancer and complained of abdominal pain, thought to be visceral pain caused by obstruction of the digestive tract. Oral intake became more difficult as the disease progressed. Despite a switch to FP from oxycodone used to treat the abdominal pain and an increase in the dose, pain relief was not achieved. Then, we undertook a partial opioid rotation to continuous intravenous infusion of morphine hydrochloride, which provided adequate pain control. Discussion: One possible reason for the pain relief in this patient is suppression of the gastrointestinal motility by morphine. When adequate pain relief cannot be achieved with one opioid, opioid rotation should be considered. We concluded that the opioid rotation should, however, be performed in a stepwise manner. Palliat Care Res 2009; 4(1): 307-311

The mandibular condyle formation during temporomandibular joint (TMJ) development exhibits endochondral bone formation, and the elongation process is dependent on the normal cartilage proliferation and differentiation. Retinoids are important for maturation of growth-plate chondrocytes, but the identity of their downstream effectors remains unclear. In this study, we carried out a series of studies at the cellular, biochemical, and molecular levels to determine whether, and if so how, retinoid signaling is related to the expression and function of Indian hedgehog (Ihh) in chondrocyte proliferation. First we analyzed the RA receptor (RAR) and Ihh expression pattern in E18 mandibular condyle. RARα and RARβ mRNA were characterized in the perichondrium around the condyle, whereas RARγ mRNA was expressed in the immature and prehypertrophic chondrocytes and the expression was overlapped with Ihh gene expression. Next we established a high-density culture model of chick cephalic chondrocytes in the prehypertrophic stage. We found that all-trans retinoic acid (RA) induced Ihh mRNA gene expression in this system. The RA pan-antagonist Ro 41-5253 inhibited both endogenous and RA-induced Ihh mRNA in a dose-dependent manner. The Ihh mRNA expression induced by RA required de novo protein synthesis, and was mediated by RARγ. Immunoblots showed that the prehypertrophic chondrocytes contained sizable levels of phosphorylated p38 mitogen-activated protein (MAP) kinase that were time- and dose-dependently increased by the RA treatment. Experimental p38 inhibition led to a severe drop in baseline and RA-stimulated Ihh expression. Exogenous recombinant Ihh stimulated the proliferation of proliferating chondrocytes, whereas RA inhibited the proliferation of these chondrocytes through p38 MAPK. Retinoids appear to play a primary role in controlling both the expression and function of Ihh in prehypertrophic chondrocytes and do so via p38 MAP kinase.