Activation of Satellite Glial Cells in Rat Trigeminal Ganglion after Upper Molar Extraction

The neurons in the trigeminal ganglion (TG) are surrounded by satellite glial cells (SGCs), which passively support the function of the neurons, but little is known about the interactions between SGCs and TG neurons after peripheral nerve injury. To examine the effect of nerve injury on SGCs, we investigated the activation of SGCs after neuronal damage due to the extraction of the upper molars in rats. Three, 7, and 10 days after extraction, animals were fixed and the TG was removed. Cryosections of the ganglia were immunostained with antibodies against glial fibrillary acidic protein (GFAP), a marker of activated SGCs, and ATF3, a marker of damaged neurons. After tooth extraction, the number of ATF3-immunoreactive (IR) neurons enclosed by GFAP-IR SGCs had increased in a time-dependent manner in the maxillary nerve region of the TG. Although ATF3-IR neurons were not detected in the mandibular nerve region, the number of GFAP-IR SGCs increased in both the maxillary and mandibular nerve regions. Our results suggest that peripheral nerve injury affects the activation of TG neurons and the SGCs around the injured neurons. Moreover, our data suggest the existence of a neuronal interaction between maxillary and mandibular neurons via SGC activation

Correlation between the Appearance of Neuropeptides in the Rat Trigeminal Ganglion and Reinnervation of the Healing Root Socket after Tooth Extraction

The neuropeptide substance P (SP) modulates bone metabolism. This study examined the temporal appearance of the neuropeptides SP and brain-derived nerve growth factor (BDNF) and their receptors (neurokinin-1 receptor (NK(1)-R) and Trk B, respectively) in the rat trigeminal ganglion to investigate the role of neuropeptides in healing after tooth extraction. Rats were anesthetized and their upper right first molars were extracted; the rats were sacrificed 3 hours and 1–21 days after extraction. Their trigeminal ganglion and maxilla were removed, and cryosections were prepared and immunostained using specific antibodies against SP, BDNF, NK(1)-R, and Trk B. In the tooth sockets after extraction, new bone and a few SP-­immunoreactive nerve fibers were first seen at day 7, and bone completely filled the sockets at day 21. In the trigeminal ganglion, the proportions of NK(1)-R-, BDNF-, and Trk B-immuno­reactive neurons changed similarly, i.e., they initially decreased, increased rapidly to ­maximum levels by day 3, and then decreased gradually to control levels until 21 days. These findings suggest that the appearance of neuropeptides in the trigeminal ganglion, the reinnervation of SP-immunoreactive nerve fibers, and bone repair in the tooth socket during healing after extraction were correlated

Long-term effect of cinacalcet hydrochloride on abdominal aortic calcification in patients on hemodialysis with secondary hyperparathyroidism

Background: Secondary hyperparathyroidism (SHPT) is one of the common complications in dialysis patients, and is associated with increased risk of vascular calcification. The effects of cinacalcet hydrochloride treatment on bone and mineral metabolism have been previously reported, but the benefit of cinacalcet on vascular calcification remains uncertain. The aim of this study was to evaluate the impact of cinacalcet on abdominal aortic calcification in dialysis patients. Subjects and methods: Patients were on maintenance hemodialysis with insufficiently controlled SHPT (intact parathyroid hormone [PTH] >180 pg/mL) by conventional therapies. All subjects were initially administered 25 mg cinacalcet daily, with concomitant use of calcitriol analogs. Abdominal aortic calcification was annually evaluated by calculating aortic calcification area index (ACAI) using multidetector computed tomography (MDCT), from 12 months before to 36 months after the initiation of cinacalcet therapy. Results: Twenty-three patients were analyzed in this study. The mean age was 59.0±8.7 years, 34.8% were women, and the mean dialysis duration was 163.0±76.0 months. After administration of cinacalcet, serum levels of intact PTH, phosphorus, and calcium significantly decreased, and mean Ca × P values significantly decreased from 67.4±7.9 mg2/dL2 to 52±7.7 mg2/dL2. Although the ACAI value did not decrease during the observation period, the increase in ACAI between 24 months and 36 months after cinacalcet administration was significantly suppressed. Conclusion: Long-term administration of cinacalcet was associated with reduced progression of abdominal aortic calcification, and achieving appropriate calcium and phosphorus levels may reduce the rates of cardiovascular events and mortality in patients on hemodialysis

Macrophage colony-stimulating factor enhances rituximab-dependent cellular cytotoxicity by monocytes

医薬保健研究域医学系Recent studies suggest that monocytes are the dominant effectors by which rituximab induces cell death in B-cell lymphoma. Because macrophage colony-stimulating factor (M-CSF) can enhance the cytotoxicity of monocytes, the authors examined whether this growth factor can enhance their ability to kill lymphoma cells in vitro. Monocytes derived from a healthy volunteer were cultured for 48 h in the presence or absence of M-CSF. Monocytes stimul ated with M-CSF were significantly more cytotoxic to Daudi B-cell lymphomas than unstimulated monocytes. Flow cytometry revealed that M-CSF increased monocyte expression of Fcγ receptors III and I by 1.6- and 1.5-fold, whereas the expression of Fcγ receptor II remained unchanged. These results suggest that pretreatment with M-CSF can improve the therapeutic efficacy of rituximab against intractable CD20+ lymphoma. © 2007 Japanese Cancer Association

Catalyst deactivation of a silica-supported bismuth-molybdenum complex oxide and the related complex oxides for the oxidative dehydrogenation of 1-butene to 1,3-butadiene

This study was an examination of the catalyst deactivation of a silica-supported bismuth-molybdenum complex oxide, and that of catalysts used in the absence of bismuth, for the oxidative dehydrogenation of 1-butene. Due to the detection of deactivation, the molar ratio of 1-butene against oxygen in the reactant gas was adjusted to a ratio similar to that used in industrial processes where reaction temperatures average 100 K higher. Regardless of the presence or absence of bismuth in the catalysts, the conversion of 1-butene was decreased by 6 h on-stream. Both the progress of the coking from the inlet to the outlet of the catalyst and the reduction of molybdenum in the catalysts directly contributed to the deactivation. X-ray photoelectron spectrometry revealed that a greater reduction of molybdenum in the near-surface region and a smaller partial pressure of oxygen (P(O2)) in the reactant gas, although the molybdenum on the surface was not reduced at all. This indicated that the lattice oxygen was pumped from the near-surface region to the surface during the reaction and the oxygen-poor conditions of the near-surface region both in the gas and catalyst phases were formed at a smaller P(O2), which resulted in the enhancements of both the reduction of molybdenum and that of coking. Based on the thermogravimetric analysis, the silica-supported bismuth-molybdenum complex oxide used at P(O2) = 4.1 kPa (color of the catalyst = black) was increased in weight while that used at P(O2) = 16.4 kPa (color of the catalyst = gray) showed a weight decrease, which indicated that the weight decrease caused by the reduction in molybdenum in the near-surface region used at 4.1 kPa was greater than the weight increase from the coking. It was concluded that the reduction in molybdenum followed by the coking on the catalyst surface were the main factors in the catalyst deactivation