Objective To observe the sedative effectiveness of dexmedetomidine (DEX) in digital subtraction angiography (DSA),and to investigate the optimal and safe administration dose.Methods Seventy-five patients undergoing DSA were divided into three groups by random digits table with 25 cases each group.Three groups were treated with constant infusion of DEX by micro-pump 10 min before surgery with the same dose of saline.Then group A,B,C respectively were given 0.3,0.5,0.7 μg/ (kg·h) of the maintenance infusion rate,and stop infusion 10 min before the end of the surgery.At administration (T0),10 (T1),20 (T2) and 30 (T3) min after administration,10 min after surgery (T4),the heart rate (HR),mean arterial pressure (MAP),peripheral oxygen saturation (SpO2),Ramsay score,number of cases that appeared body movement were recorded,and their forgotten degree of operating memory were compared.Results The HR,MAP in three groups at T1-T3 was significandy lower than that at T0 (P＜ 0.05),T4 levels returned to T0 (P＞ 0.05).The HR,MAP in group C at T2,T3 was significantly lower than that in group A and group B at the same time (P ＜ 0.05).The Ramsay score in three groups at T2,T3 was significantly higher than that at T0(P ＜0.05),group B and group C at T2,T3 was significantly higher than that in group A at the same time (P ＜0.05).The SpO2 in three groups at each time point compared within and among groups was no significant difference (P ＞ 0.05).Group B and group C intraoperative involuntary movement in response patients were significantly less than in group A (5,3 cases vs.10 cases).Group A and group C surgery requires intervention patients was significantly more than in group B (8,10 cases vs.3 cases).Group B and group C amnesia grade Ⅲ rate was significantly higher than that in group A [64％ (16/25),72％ (18/25) vs.40％(10/25),P ＜ 0.05].Conclusion Infusion with 0.5 μ g/(kg· h) DEX 10 min after intravenous injection with 0.5 μ g/kg can get a better sedative effect,stable vital signs and less intraoperative adverse memory,and it can also improve patients' comfortable degree,which is safe and appropriate sedative dosage in DSA.

BACKGROUND:Cortical electrical stimulation has achieved good effects in treatment of stroke through animal and clinical experiments.
OBJECTIVE:To observe the effects of a ful y implanted cortical electrical stimulation device with long time, low intensity and various frequencies stimulation protocols on the neurological function recovery in a rat model of local cerebral infarction.
METHODS:The cerebral infarction model was established through middle cerebral artery occlusion in 60 Sprague-Dawley adult male rats. Forty rats with 1-3 points by Bederson scale were detected with magnetic resonance imaging, which was used to confirm cortex infarction and to identify a location for implantation of stimulating electrode over the peri-infarct cortex. Twenty-three rats with cortex infarction were randomly divided into cortical electrical stimulation group (CES group, n=13) and no stimulation group (NS group;n=10). The device was implanted on 6 days after middle cerebral artery occlusion, and the stimulation was given for 16 days. The stimulation program consists of two sessions lasting half an hour each in the morning and in the afternoon respectively. Stimulator delivered biphasic charge balanced pulses (pulse width=200μs) with various frequencies of 50 Hz, 20 Hz and 5 Hz within 10 second blocks and then repeated. The rats of NS group were implanted with the device, but received no electrical stimulation. The behavioral tests, includingforelimb use asymmetry test and foot fault test were performed at 2 and 16 days after implantation. Final y, al of the devices were taken out to test if they were normal y working and al of the rats were sacrificed for hematoxylin-eosin staining, which can reflect the structure of peri-infarct cortex and cellmorphology.
RESULTS AND CONCLUSION:There was only one stimulator in CES group cannot normal y work, and the remaining 22 ones worked wel . The skin covered the implanted stimulator was slightly ulcerated in one rat, and the incisions of the other rats were healed wel . Hematoxylin-eosin staining showed clear and intact structure in peri-infarction cortex (i.e., electrodes were implanted at the cortex), neurons arranged in neat rows, with abundant neuronal cytoplasm and clear nucleolus. The glial cells have complete structures, and there was no edema in the intercellular spaces. Foot-fault and forelimb use asymmetry tests showed the improved neurological function in rats of CES group than that of NS group. We designed a ful-implanted cortical electrical stimulator used in cerebral ischemic rats, and established an implanted method with long time, low intensity and various frequencies pulsed electrical stimulation. The results indicated the stimulation pattern in our study is safe and effective, and it can significantly promote functional recovery in local cerebral infarction rats.

BACKGROUNDGallbladder carcinoma (GBC) has a high mortality rate, requiring synergistic anti-tumor management for effective treatment. The myxoma virus (MYXV) exhibits a modest clinical value through its oncolytic potential and narrow host tropism.

METHODSWe performed viral replication assays, cell viability assays, migration assays, and xenograft tumor models to demonstrate that bone marrow-derived stem cells (BMSCs) may enhance efficiency of intravenous MYXV delivery.

RESULTSWe examined the permissiveness of various GBC cell lines towards MYXV infection and found two supported single and multiple rounds of MYXV replication, leading to an oncolytic effect. Furthermore, we found that BMSCs exhibited tropism for GBC cells within a Matrigel migration system. BMSCs failed to affect the growth of GBC cells, in terms of tumor volume and survival time. Finally, we demonstrated in vivo that intravenous injection of MYXV-infected BMSCs significantly improves the oncolytic effect of MYXV alone, almost to the same extent as intratumoral injection of MYXV.

CONCLUSIONThis study indicates that BMSCs are a promising novel vehicle for MYXV to clinically address gallbladder tumors.

Animals ; Bone Marrow Cells ; cytology ; Cell Movement ; physiology ; Cell Survival ; physiology ; Female ; Gallbladder Neoplasms ; therapy ; virology ; Humans ; Immunohistochemistry ; Mice ; Myxoma virus ; pathogenicity ; Stem Cells ; cytology ; physiology ; Virus Replication ; physiology ; Xenograft Model Antitumor Assays