Background Unlike the right internal jugular vein (RIJV), there is a paucity of data regarding the effect of the Trendelenburg position on the left internal jugular vein (LIJV). The purpose of this study is to investigate the cross-sectional area (CSA) of the LIJV and RIJV and their response to the Trendelenburg position using two-dimensional ultrasound in adult subjects.MethodsThis study enrolled fifty-eight patients with American Society of Anesthesiologists physical status class I-II who were undergoing general anesthesia. CSAs of both the RIJV and LIJV were measured with a two-dimensional ultrasound in the supine position and then in a 10° Trendelenburg position.ResultsIn the supine position, the transverse diameter, anteroposterior diameter, and CSA of the RIJV were significantly larger than those of the LIJV (P < 0.001). Of 58 patients, the RIJV CSA was larger than the LIJV CSA in 43 patients (74.1%), and the LIJV CSA was larger than the RIJV CSA in 15 patients (25.9%). In the Trendelenburg position, CSAs of the RIJV and LIJV increased 39.4 and 25.5%, respectively, compared with the supine position. However, RIJV changed at a rate that was significantly greater than that of the LIJV (P < 0.05). Of 58 patients, the RIJV CSA was larger than the LIJV CSA in 48 patients (82.8%), and the LIJV CSA was larger than the RIJV CSA in 10 patients (17.2%).ConclusionsIn supine position, the RIJV CSA was larger than the LIJV CSA. The increased CSA in the Trendelenburg position was greater in the RIJV than the LIJV.

An 81-year-old male patient was scheduled for a laparoscopic cholecystectomy due to acute cholecystitis. About 50 minutes into the operation, the arterial blood pressure suddenly decreased and ventricular fibrillation appeared on the electrocardiography. The patient received cardiopulmonary resuscitation and recovered a normal vital sign. We suspected a carbon dioxide embolism as the middle hepatic vein had been injured during the surgery. We performed a transesophageal echocardiography and were able to confirm the presence of multiple gas bubbles in all of the cardiac chambers. After the operation, the patient presented a stable hemodynamic state, but showed weaknesses in the left arm and leg. There were no acute lesions except for a chronic cerebral cortical atrophy and chronic microvascular encephalopathy on the postoperative brain-computed tomography, 3D angiography and magnetic resonance image. Fortunately, three days after the operation, the patient's hemiparesis had entirely subsided and he was discharged without any neurologic sequelae.

BackgroundG protein-coupled receptor, family C, group 5 (GPRC5B), a retinoic acid-inducible orphan G-protein-coupled receptor (GPCR), is a member of the group C metabotropic glutamate receptor family proteins presumably related in non-canonical Wnt signaling. In this study, we investigated altered GPRC5B expression in the dorsal horn of the spinal cord after spinal nerve injury and its involvement in the development of neuropathic pain.MethodsAfter induction of anesthesia by intraperitoneal injection of pentobarbital (35 mg /kg), the left L5 spinal nerve at the level of 2 mm distal to the L5 DRG was tightly ligated with silk and cut just distal to the ligature. Seven days after nerve injury, animals were perfused with 4% paraformaldehyde, and the spinal cords were extracted and post-fixed at 4℃ overnight. To identify the expression of GPRC5B and analyze the involvement of GPRC5B in neuropathic pain, immunofluorescence was performed using several markers for neurons and glial cells in spinal cord tissue.ResultsAfter L5 spinal nerve ligation (SNL), the expression of GPRC5B was decreased in the ipsilateral part, as compared to the contralateral part, of the spinal dorsal horn. SNL induced the downregulation of GPRC5B in NeuN-positive neurons in the spinal dorsal horn. However, CNPase-positive oligodendrocytes, OX42-positive microglia, and GFAP-positive astrocytes were not immunolabeled with GPRC5B antibody in the spinal dorsal horn.ConclusionsThese results imply that L5 SNL-induced GPRC5B downregulation may affect microglial activation in the spinal dorsal horn and be involved in neuropathic pain.

CLB2.0, a constituent of PM, induces secretion of multiple cytokines and chemokines that regulate airway inflammation. Specifically, IL-6 upregulates CLB2.0-induced MUC5AC and MUC1 expression. Interestingly, of the tight junction proteins examined, claudin-1 expression was inhibited by CLB2.0. While the overexpression of claudin-1 decreased CLB2.0-induced MUC5AC expression, it increased the expression of the anti-inflammatory mucin, MUC1. CLB2.0-induced IL-6 secretion was mediated by ROS. The ROS scavenger N-acetylcysteine inhibited CLB2.0-induced IL-6 secretion, thereby decreasing the CLB2.0-induced MUC5AC expression, whereas CLB2.0-induced MUC1 expression increased. CLB2.0 activated the ERK1/2 MAPK via a ROS-dependent pathway. ERK1/2 downregulated the claudin-1 and MUC1 expressions, whereas it dramatically increased CLB2.0-induced MUC5AC expression. These findings suggest that CLB2.0-induced ERK1/2 activation acts as a switch for regulating inflammatory conditions though a ROS-dependent pathway. Our data also suggest that secreted IL-6 regulates CLB2.0-induced MUC5AC and MUC1 expression via ROS-mediated downregulation of claudin-1 expression to maintain mucus homeostasis in the airway.

Mucus secretion is often uncontrolled in many airway inflammatory diseases of humans. Identifying the regulatory pathway(s) of mucus gene expression, mucus overproduction, and hypersecretion is important to alleviate airway inflammation in these diseases. However, the regulatory signaling pathway controlling mucus overproduction has not been fully identified yet. In this study, we report that the ATP/P2Y2 complex secretes many cytokines and chemokines to regulate airway inflammation, among which IL-1 receptor antagonist (IL-1ra) downregulates MUC5AC gene expression via the inhibition of Gαq-induced Ca2+ signaling. IL-1ra inhibited IL-1α protein expression and secretion, and vice versa. Interestingly, ATP/P2Y2-induced IL-1ra and IL-1α secretion were both mediated by PLCβ3. A dominant-negative mutation in the PDZ-binding domain of PLCβ3 inhibited ATP/P2Y2-induced IL-1ra and IL-1α secretion. IL-1α in the presence of the ATP/P2Y2 complex activated the ERK1/2 pathway in a greater degree and for a longer duration than the ATP/P2Y2 complex itself, which was dramatically inhibited by IL-1ra. These findings suggest that secreted IL-1ra exhibits a regulatory effect on ATP/P2Y2-induced MUC5AC gene expression, through inhibition of IL-1α secretion, to maintain the mucus homeostasis in the airway. Therefore, IL-1ra could be an excellent modality for regulating inflamed airway microenvironments in respiratory diseases.