The present study was designed to provide more extensive information on the effects of chronic in vivo β-adrenergic stimulation as produced in two different fashions, one through exercise training and the other through the chronic administration of isoproterenol, on the characteristics of β-adrenergic receptors (β-AR) in rat adipocyte membranes.
1. The chronic administration of isoproterenol (2.5 mg/kg BW sc, daily for 21 days; IPR-treatment) significantly reduced lipolysis induced by noradrenaline in isolated adipocytes. However, exercise training (8 weeks of treadmill running) significantly increased the lipolytic response of adipocytes to noradrenaline.
2. IPR-treatment significantly decreased the percentage of the high affinity state (%R_H) and increased the dissociation constants of the high affinity state (K_H) of β-AR in computer modeling of (-) -noradrenaline competition curves. However, exercise training significantly increased %R_H.
In conclusion, IPR-treatment reduced the lipolytic response of adipocytes to noradrenaline, at least partially, which resulted in the decreased formation of the high affinity state of β-AR. Exercise training may enhance the lipolytic ability of adipocytes to catecholamines through facilitating the formation of the high affinity state of β-AR.

In this study, it has been investigated whether chronic isoproterenol treatments can reproduce the effect of exercise-training on rat epididymal adipose tissue (WAT) .
1. Exercise-training (treadmill running 5 days/week for 8 weeks) reduced the weight-gain, the amount of WAT and the mean daily food intake compared with control. Exercise-training caused hypertrophy of heart and submandibular glands.
2. Chronic isoproterenol-treatments (2.5 mg/100 g body weight/day sc for 6 days) reduced the body weight and the amount of WAT and caused hypertrophy of heart and submandibular glands compared with saline (0.9%) treated rats.
3. Exercise-training markedly increased lipolysis induced by adrenaline (5.5 μM) in WAT segments, and slightly increased lipolysis induced by noradrenaline (5.5 μM) and caffeine (3 mM) . However, lipolysis induced by ACTH (0.5 μM) was markedly decreased.
4. Chronic isoproterenol-treatments markedly increased lipolysis induced by each lipolytic agent.
5. Chronic isoproterenol-treatments mimicked the effect of exercise-training on the weight of various organs, but not on lipolysis induced by ACTH.
6. Chronic isoproterenol-treatments could not reproduce all effects of exercisetraining on rat WAT. Therefore, these results suggest that the response of rat WAT to exercise-training is mediated not only by the beta effect of catacholamine but also by various hormonal factors, and further suggest that it is difficult to reproduce the effect of physiological nerve stimulation only by chronic injections of a neurotransmitter.

The present study was designed to provide more extensive information on the effects of chronic in vivo β-adrenergic stimulation as produced in two different fashions, one through exercise training and the other through the chronic administration of isoproterenol, on the characteristics of β-adrenergic receptors (β-AR) in rat adipocyte membranes.
1. The chronic administration of isoproterenol (2.5 mg/kg BW sc, daily for 21 days; IPR-treatment) significantly reduced lipolysis induced by noradrenaline in isolated adipocytes. However, exercise training (8 weeks of treadmill running) significantly increased the lipolytic response of adipocytes to noradrenaline.
2. IPR-treatment significantly decreased the percentage of the high affinity state (%R_H) and increased the dissociation constants of the high affinity state (K_H) of β-AR in computer modeling of (-) -noradrenaline competition curves. However, exercise training significantly increased %R_H.
In conclusion, IPR-treatment reduced the lipolytic response of adipocytes to noradrenaline, at least partially, which resulted in the decreased formation of the high affinity state of β-AR. Exercise training may enhance the lipolytic ability of adipocytes to catecholamines through facilitating the formation of the high affinity state of β-AR.

Effects of environmental (cold) stress and aging on cells in monocyte/macrophage lineage were investigated. We demonstrated that immune suppressive states seen in acute cold-stressed mice (8-10 weeks of age) is attributable to FcγRIIbright suppressor macrophages. Serum corticosterone levels were markedly increased in acute cold-stressed mice. In addition, expression of glucocorticoids (GC) receptor mRNA was observed in FcγRIIbright cells from these mice. The increase of FcγRIIbright cells in peritoneal exudate cells caused by acute cold stress was inhibited by adrenalectomy or administration of a saturating amount of the GC antagonist RU 38486 (mifepristone). On the contrary, administration of the GC agonist, dexamethasone, markedly increased the proportion of FcγRIIbright cells in peritoneal exudate cells of control mice. These results suggest that the generation of FcγRIIbright suppressor cells of monocyte/macrophage lineage by acute cold stress was mediated by action of GC through the GC receptor. We likewise found that the proportion of FcγRIIbright suppressor macrophages is increased in aged mice (22-24 months of age). Meanwhile, activated macrophages which function as antigen presenting cells were decreased in aged rats. Both the basal corticosterone concentrations in serum and the expression of mRNA for GC receptor in peritoneal macrophages increased significantly in aged animals, suggesting that these populational and functional changes of macrophages in aged animals were mediated, in part, by the increased basal levels of GC. This is probably being responsible for immunosenescence.
Neisseria gonorrhoeae ; Laboratory mice ; Acute ; Macrophages ; receptor

Effects of environmental (cold) stress and aging on cells in monocyte/macrophage lineage were investigated. We demonstrated that immune suppressive states seen in acute cold-stressed mice (8-10 weeks of age) is attributable to FcγRII(bright) suppressor macrophages. Serum corticosterone levels were markedly increased in acute cold-stressed mice. In addition, expression of glucocorticoids (GC) receptor mRNA was observed in FcγRII(bright) cells from these mice. The increase of FcγRII(bright) cells in peritoneal exudate cells caused by acute cold stress was inhibited by adrenalectomy or administration of a saturating amount of the GC antagonist RU 38486 (mifepristone). On the contrary, administration of the GC agonist, dexamethasone, markedly increased the proportion of FcγRII(bright) cells in peritoneal exudate cells of control mice. These results suggest that the generation of FcγRII(bright) suppressor cells of monocyte/macrophage lineage by acute cold stress was mediated by action of GC through the GC receptor. We likewise found that the proportion of FcγRII(bright) suppressor macrophages is increased in aged mice (22-24 months of age). Meanwhile, activated macrophages which function as antigen presenting cells were decreased in aged rats. Both the basal corticosterone concentrations in serum and the expression of mRNA for GC receptor in peritoneal macrophages increased significantly in aged animals, suggesting that these populational and functional changes of macrophages in aged animals were mediated, in part, by the increased basal levels of GC. This is probably being responsible for immunosenescence.

Objective: To treat vertebral fractures with posterior wall injury in the elderly, vertebral bone grafting is generally performed through a posterior transpedicular approach, combined with pedicle screw fixation. An autologous bone is ideal to treat this disorder. However, harvesting autologous bones from the elderly with osteoporosis is limited by the amount and quality of available autologous bone. Thus, we developed a bone-grafting substitute. The newly developed unidirectional porous β-tricalcium phosphate, with a porosity of 57% (UDPTCP; Affinos®, Kuraray Co., Ltd., Tokyo, Japan), is used in the bone-grafting procedure. This is the first report of UDPTCP used as an artificial bone graft in patients with an acute vertebral burst fracture.Materials and Methods: UDPTCP (mean: 4.2 g) was implanted through the pedicle, and posterior instrumentation was achieved with pedicle screws in five elderly patients. Resorption of UDPTCP and substitution with the autologous bone were evaluated on computed tomography (CT) and plain X-ray performed immediately and at 3, 6, and 12 months after the operation.Results: In case 1, the pedicle screws did not loosen, and UDPTCP was completely resorbed and replaced with the autologous bone at 3 postoperative months. In the other four cases, although the pedicle screws or the caudal part loosened because of osteoporosis, resorption of UDPTCP was observed at 3 postoperative months. At 6 postoperative months, progressive substitution with the autologous bone was confirmed, and at 12 postoperative months, formation of the good autologous bone was confirmed.Conclusion: This preliminary case series demonstrated that the newly developed UDPTCP shows good clinical potential as a bone-graft substitute for acute vertebral burst fractures in the elderly, including patients with osteoporosis.