Transvenous retrograde AVM embolization: Indications, techniques, complications and outcomes.

Objective Transvenous retrograde arteriovenous malformation (AVM) embolization (TRAE) has been proposed. The present study was to review the techniques, their conjunctions and effectiveness. Methods Eligible related articles were identified by searching the PubMed and Web of Science databases using "transvenous" and "arteriovenous malformation." Results A total of 16 eligible studies, with 60 cases of AVM treated with TRAE, were analyzed. Prior to TRAE procedure, transarterial Onyx 18 was performed in 23 (38.3%), cyanoacrylate in three (5%) and coiling in two (3.3%), neurosurgery in one (1.7%) and radiosurgery in three (5%). These prior treatments were used to reduce the size of the nidus to <3 cm and TRAE was performed. One anterior choroidal artery aneurysm was coiled before TRAE. Systemic hypotension (blood pressure<100 mmHg) occurred in six (10%) patients and local hypotension (proximal arterial temporary balloon protection) in five (8.3%) patients. Complete obliteration was achieved in 56 (93.3%) AVMs, four (6.7%) with residual, of which one was supplemented with radiosurgery. During mean one-year follow-up (1 month to 3.2 years), there were five cases (8.3%) of permanent disability and one (1.7%) mortality resulting from initial hemorrhage. Fifty-four (90%) patients were independent (mRS ≤ 2) at follow-up. Ruptured AVMs and Spetzler-Martin I-III were associated with a high cure rate. Conclusion According to previous reports, selected AVMs could undergo TRAE. TRAE is safe and curative with Onyx after the nidus size is reduced sufficiently by transarterial embolization, neurosurgery or radiosurgery, with or without the aid of proximal arterial temporary balloon protection.

Interactions of hydroxyapatite with proteins and its toxicological effect to zebrafish embryos development.

The increased application of nanomaterials has raised the level of public concern regarding possible toxicities caused by exposure to nanostructures. The interactions of nanosized hydroxyapatite (HA) with cytochrome c and hemoglobin were investigated by zeta-potential, UV-vis, fluorescence and circular dichroism. The experimental results indicated that the interactions were formed via charge attraction and hydrogen bond and obeyed Langmuir adsorption isotherm. The two functional proteins bridged between HA particles to aggregate into the coralloid form, where change of the secondary structure of proteins occurred. From effects of nanosized HA, SiO(2) and TiO(2) particles on the zebrafish embryos development, they were adsorbed on the membrane surface confirmed by the electronic scanning microscopy. Nano-HA aggregated into the biggest particles around the membrane protein and then caused a little toxicity to development of zebrafish embryos. The SiO(2) particles were distributed throughout the outer surface and caused jam of membrane passage, delay of the hatching time and axial malformation. Maybe owing to the oxygen free radical activity, TiO(2) caused some serious deformity characters in the cardiovascular system.

PCP can enhance dendritic cells to present the HBsAg peptide.

AIM: To investigate the influence of paraclorophenol (pCP) on dendritic cells loading and presenting HBsAg from peripheral blood monocytes of healthy volunteers identified as hepatitis B vaccine nonresponders. METHODS: The density gradient centrifugation was performed to isolate mononuclear cells from 10 hepatitis B vaccine nonresponders. The adherent monocytes were incubated with HBsAg adding rhGM-CSF and rhIL-4 in the presence of absence of pCP for 7 days. Then the supernatant was collected for ELISA assays. The culture medium system without pCP was used as negative control and without pCP or HBsAG was named blank control. the matured DCs were co-incubated with autologous T lymphocytes for 72h and the supernatant was also collected for ELISA assays. RESULTS: In the presence of pCP, the level of IL-12 in supernate (265.68± 16.21) ng/L was significantly higher than the negative control (168.76±10.01) ng/L (P<0.05) and blank control (87±5.79)ng/L (P<0.05); after co-incubated with autologous T lymphocytes for 3 days, the level of IFN-γ with pCP (773.04±32.73) mg/L was also significantly higher than the negative control (573.59±26.11) mg/L (P<0.05) ans blank control (362.81±24.27)mg/L (P<0.05). CONCLUSION: pCP can effectively enhance the dendritic cells loading and presenting HBsAg from peripheral blood monocytes of healthy volunteers identified as hepatitis B vaccine nonresponders, which also can dramatically increase te autologous T lymphocytes response.7

Investigating the role of hypothalamic paraventricular nucleus in nociception of the rat.

The role of hypothalamic paraventricular nucleus (PVN) in nociception was investigated in the rat. Electrical stimulation of the PVN increased pain threshold, and microinjection of L-glutamate sodium into the PVN also elevated pain threshold in a dose-dependent manner, whereas cauterization of the PVN decreased pain threshold. Stimulation or cauterization of the area located within 1.0 mm of the outer perimeter of the PVN did not change pain threshold. Pituitary removal could not influence the effect of L-glutamate sodium microinjection into PVN-induced pain threshold increase. The data suggest that PVN plays a role in antinociception through the central nervous system rather than peripheral organs.

Only through the brain nuclei, arginine vasopressin regulates antinociception in the rat.

The effect of arginine vasopressin (AVP) on rat antinociception was investigated. Intraventricular injection of 50 or 100 ng AVP dose-dependently increased the pain threshold; in contrast, intraventricular injection of 10 microl anti-AVP serum decreased the pain threshold; both intrathecal injection of 200 ng AVP or 10 microl anti-AVP serum and intravenous injection of 5 microg AVP or 200 microl anti-AVP serum did not influence the pain threshold. Pain stimulation reduced AVP concentration in hypothalamic paraventricular nucleus (PVN), and elevated AVP concentration in hypothalamic supraoptical nucleus (SON) and periaqueductal gray (PAG), but no change in AVP concentration was detected in pituitary, spinal cord and serum. The results indicated that AVP regulation of antinociception was limited to the brain nuclei.

Arginine vasopressin in the caudate nucleus plays an antinociceptive role in the rat.

Our previous work has shown that arginine vasopressin (AVP) regulates antinociception through brain nuclei rather than the spinal cord and peripheral organs. The present study investigated the nociceptive effect of AVP in the caudate nucleus (CdN) of the rat. Microinjection of AVP into the CdN increased pain threshold in a dose-dependent manner, while local administration of AVP-receptor antagonist-d(CH(2))(5)Tyr(Et)DAVP decreased pain threshold. Pain stimulation elevated AVP concentration in CdN perfuse liquid. CdN pretreatment with AVP-receptor antagonist completely reversed AVP's effect on pain threshold in the CdN. The data suggest that AVP in the CdN is involved in antinociception.

Effect of arginine vasopressin in the nucleus raphe magnus on antinociception in the rat.

Previous work has shown that arginine vasopressin (AVP) regulates antinociception through brain nuclei rather than the spinal cord and peripheral organs. The present study investigated the nociceptive effect of AVP in the nucleus raphe magnus (NRM) of the rat. Microinjection of AVP into the NRM increased pain threshold in a dose-dependent manner, while local administration of AVP-receptor antagonist-d(CH2)5Tyr(Et)DAVP decreased the pain threshold. Pain stimulation elevated AVP concentration in the NRM perfuse liquid. NRM pretreatment with AVP-receptor antagonist completely reversed AVP's effect on pain threshold in the NRM. The data suggest that AVP in the NRM is involved in antinociception.

Only arginine vasopressin, not oxytocin and endogenous opiate peptides, in hypothalamic paraventricular nucleus play a role in acupuncture analgesia in the rat.

Our previous study proved that hypothalamic paraventricular nucleus (PVH) plays an important role in acupuncture analgesia. The effect of acupuncture on the concentrations of arginine vasopressin (AVP), oxytocin (OXT), leucine-enkephaline (L-Ek), beta-endorphin (beta-Ep) and dynorphinA(1-13) (DynA(1-13)) was investigated in rat PVH. Electrical acupuncture of "Zusanli" points (St. 36) 30 min increased the AVP, not OXT, L-Ek, beta-Ep and DynA(1-13) concentrations in PVH tissue using micropunch and radioimmunoassay, which showed a negative relationship between the pain threshold and AVP concentrations in PVH tissue. Electrical acupuncture could elevate the AVP concentrations in PVH perfuse liquid during acupuncture, and then reduce the AVP concentrations in PVH perfuse liquid after acupuncture. But no change in OXT, L-Ek, beta-Ep and DynA(1-13) concentrations was detected in PVH perfuse liquid. Electrical acupuncture decreased the number of AVP, not OXT, L-Ek, beta-Ep and DynA(1-13) immunoreactive cells in PVH using immunocytochemistry. The results suggested that only AVP, not OXT and endogenous opiate peptides in PVH involved acupuncture analgesia in the rat.

Through the central V2, not V1 receptors influencing the endogenous opiate peptide system, arginine vasopressin, not oxytocin in the hypothalamic paraventricular nucleus involves in the antinociception in the rat.

Our previous study has proven that hypothalamic paraventricular nucleus (PVN) played a role in the antinociception. The central bioactive substances involving in the PVN regulating antinociception were investigated in the rat. The results showed that electrical stimulation of the PVN increased the pain threshold, and L-glutamate sodium injection into the PVN elevated the pain threshold, but the PVN cauterization decreased the pain threshold; pain stimulation raised the arginine vasopressin (AVP), not oxytocin (OXT), leucine-enkephalin (L-Ek), beta-endorphin (beta-Ep) and DynorphinA1-13 (DynA1-13) concentrations in the PVN tissue using micropunch method, heightened AVP, L-Ek, beta-Ep and DynA1-13, not OXT concentrations in the PVN perfuse liquid, and reduced the number of AVP-, not OXT, L-Ek, beta-Ep and DynA1-13-immunoreactive neurons in the PVN especially in the posterior magnocellular part of the PVN using immunocytochemistry. There was a negative relationship between the PVN AVP concentration and the pain threshold; pain stimulation enhanced the AVP, not OXT mRNA expression in the PVN using in situ hybridization and RT-PCR; intraventricular injection of anti-AVP serum completely reversed L-glutamate sodium injection into the PVN-induced antinociception, and administration of naloxone - the opiate peptide antagonist, partly blocked this L-glutamate sodium effect, but anti-OXT serum pretreatment did not influence this L-glutamate sodium effect; L-glutamate sodium injection into the PVN-induced analgesia was inhibited by V2 receptor antagonist - d(CH2)5[D-Ile2, Ile4, Ala-NH2(9)]AVP, not V1 receptor antagonist - d(CH2)5Tyr(Me)AVP. The data suggested that the PVN was limited to the central AVP, not OXT, which was through V2, not V1 receptors influencing the endogenous opiate peptide system, to regulate antinociception.

Through central arginine vasopressin, not oxytocin and endogenous opiate peptides, glutamate sodium induces hypothalamic paraventricular nucleus enhancing acupuncture analgesia in the rat.

Our previous study proved that the hypothalamic paraventricular nucleus (PVH) plays an important role in acupuncture analgesia. The neuropeptides involving in the PVH regulation of acupuncture analgesia was investigated in the rat. The changes of pain threshold, which was induced by electrical acupuncture of "Zusanli" points (St. 36), were measured as acupuncture analgesia. Microinjection of l-glutamate sodium into the PVH, which only excites the PVH neurons, could dose-dependently enhance the acupuncture analgesia, but microinjection of l-glutamate sodium into the area nearby the PVH did not alter acupuncture analgesia. Removing pituitary did not influence this effect of l-glutamate sodium. Microinjection of l-glutamate sodium into the PVH only increased the arginine vasopressin (AVP), not oxytocin (OXT), leucine enkephaline (L-Ek), beta-endorphine (beta-Ep) and dynorphinA(1-13) (DynA(1-13)) concentrations in the PVH perfuse liquid using radioimmunoassay. Intraventricular injection of anti-arginine vasopressin serum (AAVPS) could completely reverse the effect of microinjection of l-glutamate sodium into the PVH enhancing acupuncture analgesia. Intraventricular injection of naloxone, one opiate peptide antagonist, partly attenuated this effect of l-glutamate sodium, and intraventricular of anti-oxytocin serum (AOXTS) did not change this effect of l-glutamate sodium. The results suggested that l-glutamate sodium induces the PVH enhancing acupuncture analgesia only through AVP, not OXT and endogenous opiate peptides in central nervous system.