Ultrasound-guided superficial cervical plexus block combined with clavipectoral fascial plane block or interscalene brachial plexus block in clavicle surgery: a single-centre, double-blind, randomized controlled trial.

The sensory innervation of the clavicle is complex, and the best regional block technology for clavicular surgery has yet to be determined. The purpose of this study was to compare the application of ultrasound-guided superficial cervical plexus block combined with clavipectoral fascial plane block verses interscalene brachial plexus block in clavicular surgery. Fifty patients undergoing internal fixation surgery for elective clavicle fractures were randomly divided into two groups (n = 25 for each group): group I and group II. Superficial cervical plexus block combined with clavipectoral fascial plane block was used in group I, and superficial cervical plexus block combined with interscalene brachial plexus block was used in group II. The primary outcome measure was the duration of analgesia. The duration of analgesia in group I was significantly longer than that in group II (P < 0.05). The modified Bromage scale function score in group II was lower than that in group I (P < 0.01). There was no significant difference in the skin acupuncture pain score 30 min after block and visual analog scale (VAS) scores at 6 and 12 h after surgery. However, the 24 h VAS score in group I was lower than that in group II (P < 0.05). The incidence of diaphragmatic paralysis was significantly increased in group II (P < 0.01). Ultrasound-guided superficial cervical plexus block combined with clavipectoral fascial plane block can be used for clavicular surgery. It has a long postoperative analgesia time, can retain the motor function of the involved upper limb and does not cause hemidiaphragmatic paresis.Clinical trial number and registry URL: Clinical Trials.gov; Trial registration number: ChiCTR2000039383; Date of registration: 25 October 2020.

Ceramide mediates radiation-induced germ cell apoptosis via regulating mitochondria function and MAPK factors in Caenorhabditis elegans.

Studies about radiation damage in vivo are very significant for healthy risk assessment as well as cancer radiotherapy. Ceramide as a second messenger has been found to be related to radiation-induced apoptosis. However, the detailed mechanisms in living systems are still not fully understood. In the present study, the effects of ceramide in gamma radiation-induced response were investigated using Caenorhabditis elegans. Our results indicated that ceramide was required for gamma radiation-induced whole-body germ cell apoptosis by the production of radical oxygen species and decrease of mitochondrial transmembrane potential. Using genetic ceramide synthase-related mutated strains and exogenous C16-ceramide, we illustrated that ceramide could regulate DNA damage response (DDR) pathway to mediate radiation-induced germ cell apoptosis. Moreover, ceramide was found to function epistatic to pmk-1 and mpk-1 in MAPK pathway to promote radiation-induced apoptosis in Caenorhabditis elegans. These results demonstrated ceramide could potentially mediated gamma radiation-induced apoptosis through regulating mitochondrial function, DDR pathway and MAPK pathway.

Two Compounds Isolated From Ganglioside GM1 Promote Angiogenesis in Zebrafish.

Ganglioside has been implicated to play important roles in modulating various cell signaling and biological functions. However, the functional analysis of a single ganglioside in a zebrafish model is so far lacking. In this study, we investigated the angiogenic effects of 2 monosialoganglioside compounds isolated from GM1 in zebrafish embryos. First, we showed the tested compounds are adequate safe. Then, we found that these compounds exhibited significant proangiogenic effect through enhancement of endothelial cell proliferation, migration, and differentiation. Furthermore, the 2 compounds were proved to promote angiogenesis through, at least partially, modulating the level of Notch signaling. This study provides the novel insights into the clinical application of the 2 ganglioside compounds and GM1.

[Effect of prolonged propofol infusion on myocardial enzyme, mitochondrial cytochrome C and adenosine triphosphate in rabbits].

OBJECTIVE: To explore the effect of long-time propofol infusion on myocardial enzymes, mitochondrial cytochrome C and ATP in rabbits. 
 Methods: A total of 18 New Zealand rabbits were randomly divided into 3 groups: a control group, a propofol group and an intralipid group. The rabbits were continuously infused with 0.9% normal saline in the control group, 1% propofol in the propofol group, and 10% intralipid in the intralipid group, respectivey. The arterial blood was collected at 0, 8, 16 h and the end of experiment to examine creatine kinase (CK) and creatine kinase isoenzyme (CK-MB). In the end, the myocardial mitochondria from myocardial tissues was separated by differential centrifugation, and mitochondrial cytochrome C content and adenosine triphosphate (ATP) levels were examined by high performance liquid chromatography.
 Results: Compared with the control group, the release of cytochrome C from mitochondria were increased in the propofol group and the intralipid group (both P<0.05), but there was no significant difference between them (P>0.05). There was also no significant difference in the ATP content of the mitochondria among the 3 groups (P>0.05). The levels of CK were increased at 8, 16 and 24 h after infusion in the propofol group and the intralipid group compared with that before the infusion (all P<0.05); compared with the control group, the levels of CK were increased at 8, 16 and 24 h after infusion in the propofol group and the intralipid group (all P<0.05); compared with the intralipid group, the levels of CK were increased at 8, 16 and 24 h after infusion in the propofol group (all P>0.05); compared with the control group, the levels of CK-MB were obviously increased in the infusion of propofol for 24 h in the propofol group (P<0.05).
 Conclusion: The levels of serum CK increase after the infusion of propofol and intralipid for a long time, and the levels of CK-MB also elevate in the infusion of propofol. Propofol and intralipid can increase the release of myocardial mitochondrial cytochrome C, but they don't affect the ATP production in myocardial mitochondrial.

Up-regulation of CXCL1 and CXCR2 contributes to remifentanil-induced hypernociception via modulating spinal NMDA receptor expression and phosphorylation in rats.

BACKGROUND: It is commonly known that remifentanil exposure during anesthesia might cause postoperative hyperalgesia and promote nociceptive sensitization, but specific mechanisms remain elusive. Recently, chemokine CXCL1 is considered to be involved in inflammatory and neuropathic pain, simultaneously, CXCL1 might facilitate nociceptive process by increasing of NMDA receptor activity. Several studies have also reported that NMDA receptor activation has been associated with development of remifentanil-induce hypernociception (RIH). However, whether CXCL1 could contribute to RIH in rats remains not understood. METHODS: To investigate effect of CXCL1 and its primary receptor CXCR2 on RIH, a selective CXCR2 antagonist SB225002 was administrated intrathecally after remifentanil exposure in rats. PWT and PWL were evaluated and recorded for 48 post-infusion hours to measure mechanical and thermal hyperalgesia. Then expression and phosphorylation of NMDA receptor, CXCL1 and CXCR2 levels in dorsal horn were analyzed by Western blotting and RT-qPCR after nociceptive testing. RESULTS: We discovered that remifentanil infusion could induce postoperative mechanical and thermal hypernociception, which was effectively reversed by intrathecal delivery of SB225002. Furthermore, spinal CXCL1and CXCR2 mRNA and protein expressions were elevated after remifentanil exposure. It was also found that remifentanil infusion could up-regulate NR2B-containing NMDA receptor expression and phosphorylation in spinal cord, which was markedly inhibited by SB225002. CONCLUSION: These findings indicated that up-regulation of CXCL1 and CXCR2 might contribute to RIH via modulating spinal NR2B-containing NMDA receptor expression and phosphorylation in rats.