The genus Eurymeros Bhat (Hymenoptera, Braconidae, Alysiinae) newly recorded from China.

Background: Alysiinae Leach is a species-rich subfamily in Braconidae, of which several species play an important role in biological control. The monotypic genus Eurymerostumespiraculum Bhat, 1980 was discovered in Tibet and Yunnan provinces for the first time, representing the first record of the genus Eurymeros Bhat, 1980 (Braconidae, Alysiinae) in China. New information: The rare genus Eurymeros Bhat, 1980 (Braconidae, Alysiinae) and its only known species, E.tumespiraculum Bhat, 1980, are newly recorded from China. The morphological variation of the Chinese specimens is described and illustrated.

Sonic hedgehog signaling in spinal cord contributes to morphine-induced hyperalgesia and tolerance through upregulating brain-derived neurotrophic factor expression.

PURPOSE: Preventing opioid-induced hyperalgesia and tolerance continues to be a major clinical challenge, and the underlying mechanisms of hyperalgesia and tolerance remain elusive. Here, we investigated the role of sonic hedgehog (Shh) signaling in opioid-induced hyperalgesia and tolerance. METHODS: Shh signaling expression, behavioral changes, and neurochemical alterations induced by morphine were analyzed in male adult CD-1 mice with repeated administration of morphine. To investigate the contribution of Shh to morphine-induced hyperalgesia (MIH) and tolerance, Shh signaling inhibitor cyclopamine and Shh small interfering RNA (siRNA) were used. To explore the mechanisms of Shh signaling in MIH and tolerance, brain-derived neurotrophic factor (BDNF) inhibitor K252 and anti-BDNF antibody were used. RESULTS: Repeated administration of morphine produced obvious hyperalgesia and tolerance. The behavioral changes were correlated with the upregulation and activation of morphine treatment-induced Shh signaling. Pharmacologic and genetic inhibition of Shh signaling significantly delayed the generation of MIH and tolerance and associated neurochemical changes. Chronic morphine administration also induced upregulation of BDNF. Inhibiting BDNF effectively delayed the generation of MIH and tolerance. The upregulation of BDNF induced by morphine was significantly suppressed by inhibiting Shh signaling. In naïve mice, exogenous activation of Shh signaling caused a rapid increase of BDNF expression, as well as thermal hyperalgesia. Inhibiting BDNF significantly suppressed smoothened agonist-induced hyperalgesia. CONCLUSION: These findings suggest that Shh signaling may be a critical mediator for MIH and tolerance by regulating BDNF expression. Inhibiting Shh signaling, especially during the early phase, may effectively delay or suppress MIH and tolerance.

IL-18 Contributes to Bone Cancer Pain by Regulating Glia Cells and Neuron Interaction.

Glial cell hyperactivity has been proposed to be responsible for chronic pain, however, the mechanisms remain unclear. Interleukin (IL)-18, released from glial cells, has been reported to be involved in neuropathic pain. In this study, we investigated the role of IL-18 in bone cancer pain. Bone cancer pain was mimicked by injecting Walker-256 mammary gland carcinoma cells into the intramedullary space of the tibia in rats. Expression and location of IL-18 and the IL-18 receptor were tested. To investigate the contribution of IL-18 signaling to bone cancer pain, IL-18 binding protein and recombinant IL-18 were used. To investigate the mechanisms of glial cells effects, MK801, N-methyl-D-aspartate (NMDA) receptor inhibitor, and Src kinase-specific inhibitor PP1 were used. Tumor cell implantation (TCI) treatment increased expression of IL-18 and IL-18 receptor in spinal cord. The time course of IL-18 upregulation was correlated with TCI-induced pain behaviors. Blocking the IL-18 signaling pathway prevented and reversed bone cancer-related pain behaviors. Meanwhile, blocking IL-18 signaling also suppressed TCI-induced glial cell hyperactivity, as well as activation of GluN2B and subsequent Ca2+-dependent signaling. Spinal administration of recombinant IL-18 in naive rat induced significant mechanical allodynia, as well as GluN2B activation. However, intrathecal injection of MK801 failed to suppress recombinant IL-18-induced GluN2B phosphorylation, whereas Src kinase inhibitor PP1 significantly inhibited IL-18-induced GluN2B activation. IL-18-mediated glial-glia and glial-neuron interaction may facilitate bone cancer pain. Blocking IL-18 signaling may effectively prevent and/or suppress bone cancer pain. PERSPECTIVE: IL-18 signaling may be a new target for cancer pain therapy.

Effects of dimethyltin chloride on renal H~+K~+-ATPase and Na~+K~+-ATPase activity in rats / 中国职业医学

OBJECTIVE: To study the effects of dimethyltin chloride( DMT) on the activity of renal H~+K~+-ATPase( HKA)and Na~+K~+-ATPase( NKA) in SD rats. METHODS: i) In vitro experiment. Five specific pathogen free( SPF) healthy female SD rats were used. The kidney homogenates made with 0. 90% sodium chloride solution was added with DMT( mass concentration,1. 0 g/L) to make final concentrations of 0,1,25,125 and 625 mg/L respectively,then the HKA and NKA activities were detected by the enzyme-linked immunosorbent assay( ELISA). ii) In vivo experiment. Forty SPF healthy SD rats were divided into control group and exposure group,with 20 rats( 10 males and 10 females) in each group. The exposure group was given one-time intraperitoneal injection with DMT( 16. 000 mg / kg body weight),while the control group was given one-time intraperitoneal injection with same volume of 0. 90% sodium chloride solution. The rats were executed 1 and 24 hours after exposure. The kidney tissue was extracted to make kidney homogenates for determination of HKA and NKA activity by microplate reader. The blood from abdominal aorta was collected to measure the levels of serum K~+,Na~+and Cl-. RESULTS: i) In vitro experiment. The HKA activity was inhibited by DMT,and the effect of inhibition increased with the increase of DMT exposure dose( P < 0. 01),showing a dose-effect relationship. The DMT had no effect on NKA activity( P > 0. 05). ii) In vivo experiment. The body weight of rats at 24 hours time point in exposed group was lower than that in control group( P < 0. 01). The HKA activity of the kidney tissue in rats in exposed group was lower than that of control group( P < 0. 01). The NKA activity in kidney tissue of rats and the level serum K~+,Na~+and Cl-did not show statistical difference in main and interactive effects concerning treatment and exposure time( P > 0. 05). CONCLUSION: DMT could inhibit the HKA activity in kidney homogenates,but had no obvious effect on NKA activity.

The experimental study on porous calcium phosphate cement with bone marrow stromal cells for bone tissue engineering / 华西口腔医学杂志

<p><b>OBJECTIVE</b>To observe the biocompatibility of new biomaterials porous calcium phosphate (CPC) and ectopic bone formation of CPC with bone marrow stromal cells (BMSCs).</p><p><b>METHODS</b>The BMSCs were cultured from Beagle dog and combined with the porous CPC with the best concentration after transfect green fluorescent protein (GFP). The adhesion and growth of BMSCs on CPC were observed under inversion, fluorescence and scanning electron microscopy. The ectopic bone formation were observed at the 8th week after CPC and BMSCs were implanted subcutaneously into nude mice.</p><p><b>RESULTS</b>When BMSCs with CPC were cultured at the 1st day, cells were climbing out from CPC with normal morphology. At the 7th day cells can be seen protruding pseudopods, secretion of matrix. Bone formation could be seen histomorphologically at the 8th week.</p><p><b>CONCLUSION</b>Porous CPC has good biocompatibility and is an ideal scaffold material for bone tissue engineering.</p>