Comparison of the UEscope Video Laryngoscope with the Traditional Direct Laryngoscope in Neonates and Infants: A Randomized Clinical Trial.

The role of video laryngoscopy in adults is well established, but its role in children is still inconclusive. Previous studies on the UEscope in pediatric patients with difficult airways showed that it could reduce the time to intubation (TTI) compared to a conventional direct laryngoscope. The main objective of the current study was to investigate if the use of the UEscope could reduce the TTI in neonates and infants. Forty patients under 12 months old were recruited from a single tertiary hospital from March 2020 to September 2021 and were randomly assigned to the direct laryngoscope group (n = 19, neonates = 4, infants = 15) or UEscope group (n = 21, neonates = 6, infants = 15). Although the quality of glottic view was comparable in both groups, the TTI was significantly lower in the UEscope group in both the "intention-to-treat" (-19.34 s, 95% confidence interval = -28.82 to -1.75, p = 0.0144) and "as treated" (-11.24 s, 95% confidence interval: -21.73 to 0, p = 0.0488) analyses. The UEscope may be a better choice for tracheal intubation than conventional direct laryngoscope in neonates and infants.

Transient blood brain barrier disruption induced by oleic acid is mediated by nitric oxide.

The blood brain barrier (BBB) maintains cerebral microenvironmental homeostasis. Transient disruption of the BBB after brain fat embolism in clinical cases and animal models has been reported but the precise mechanism underlying this occurrence is unclear. In the present study, we investigated BBB alterations in rats treated oleic acid (OA) delivered intra-arterially. Following OA treatment, transient brain edema, extravasation of Evans blue and Fluorescein isothiocyanate (FITC)-labeled dextran, and loss of laminin in the affected brain area were observed. Activation of matrix metalloproteinase (MMP)-2, -3, and -13 was found in the cerebral vessels 2 h after OA administration. Expression of intercellular adhesion molecule (ICAM)-1 in the vessels and neutrophil infiltration into the brain tissue was also observed. Inducible nitric oxide synthase (iNOS) was expressed in the neutrophils and nitrotyrosine was produced mainly in the vessels. Inhibitor of iNOS activity suppressed the loss of laminin, leakage of FITC-labeled dextran and Evans blue, and activation of MMP-2 and -13. Protein level of aquaporin (AQ)-4 was increased after OA administration but was not affected by treatment with iNOS inhibitor. In conclusion, we suggest that nitric oxide (NO) contributes to OA-induced MMP activation, BBB disruption and the development of transient brain edema.

Comparison of the recovery and respiratory effects of aminophylline and doxapram following total intravenous anesthesia with propofol and remifentanil.

STUDY OBJECTIVE: To compare the effects of aminophylline and doxapram on recovery, respiration, and bispectral index (BIS) values in patients after total intravenous anesthesia (TIVA) with propofol and remifentanil. DESIGN: Prospective, randomized, blinded clinical trial. SETTING: Operating room of a university hospital. PATIENTS: 90 adult, ASA physical status 1 and 2 patients scheduled for elective laparoscopic vaginal hysterectomy. INTERVENTIONS: TIVA was performed with the induction target of remifentanil 3 ng/mL and propofol 6 µg/mL, followed by the maintenance target of remifentanil 1-3 ng/mL and propofol 3-5 µg/mL at the effect site, and with BIS scores in 40-50 range. Patients were randomized to three groups to receive intravenous (IV) aminophylline 3 mg/kg (n = 30), IV doxapram 1 mg/kg (n = 30), or normal IV saline (control; n = 30). MEASUREMENTS AND MAIN RESULTS: After administration of the study drugs, return to spontaneous ventilation differed significantly among the three groups. The times to eye opening and hand squeezing on verbal command were similar. The time to extubation was shortened in both the doxapram and aminophylline groups (P < 0.05). Tidal volumes were increased in the doxapram group at 5-14 minutes and the aminophylline group at 5-12 minutes (P < 0.05). Respiratory rates were increased at 2 to 8 minutes and then showed a decrease at the 12 to 14-minute mark in both the doxapram and aminophylline groups (P < 0.05). No difference was noted between the two groups. BIS values were increased in both the doxapram and aminophylline groups at 4-10 minutes (P < 0.05). Heart rates were increased in the doxapram group for the first 8 minutes and at 1-2 minutes in the aminophylline group (P < 0.05). CONCLUSION: Aminophylline 3 mg/kg or doxapram 1 mg/kg shortened the time to spontaneous ventilation and improved early recovery from TIVA without appreciable side effects. The more rapid emergence correlates with higher BIS values when compared with the saline control group. The arousal and respiratory effects of aminophylline were comparable to those of doxapram.

Progesterone produces antinociceptive and neuroprotective effects in rats with microinjected lysophosphatidic acid in the trigeminal nerve root.

BACKGROUND: In our present study, we studied the role of demyelination of the trigeminal nerve root in the development of prolonged nociceptive behavior in the trigeminal territory. RESULTS: Under anesthesia, the Sprague-Dawley rats were mounted onto a stereotaxic frame and 3 µL of lysophosphatidic acid (LPA, 1 nmol) was injected into the trigeminal nerve root to produce demyelination. This treatment decreased the air-puff thresholds, persisted until postoperative day 130, and then returned to the preoperative levels 160 days after LPA injection. The LPA-treated rats also showed a significant hyper-responsiveness to pin-prick stimulation. We further investigated the antinociceptive and neuroprotective effects of progesterone in rats undergoing demyelination of the trigeminal nerve root. Progesterone (8, 16 mg/kg/day) was administered subcutaneously, beginning on the operative day, for five consecutive days in the LPA-treated rats. Treatment with progesterone produced significant early anti-allodynic effects and delayed prolonged anti-allodynic effects. The expression of protein zero (P0) and peripheral myelin protein 22 (PMP22) were significantly down-regulated in the trigeminal nerve root on postoperative day 5 following LPA injection. This down-regulation of the P0 and PMP22 levels was blocked by progesterone treatment. CONCLUSIONS: These results suggest that progesterone produces antinociceptive effects through neuroprotective action in animals with LPA-induced trigeminal neuropathic pain. Moreover, progesterone has potential utility as a novel therapy for trigeminal neuropathic pain relief at an appropriate managed dose and is therefore a possible future treatment strategy for improving the recovery from injury.

Assessment of three dimensional quantitative coronary analysis by using rotational angiography for measurement of vessel length and diameter.

The aim of the study was to assess the accuracy of the three-dimensional (3D) quantitative coronary analysis (QCA) system by comparing with that of intravascular ultrasound (IVUS) QCA and two-dimensional (2D) QCA. 3D QCA, 2D QCA and IVUS QCA were performed in 45 vessel segments. The obtained values for the branch to branch segment vessel length and the proximal part of the segment vessel's lumen diameter were measured. Inter-technique agreement was analyzed using paired sample t-test and Bland-Altman analysis. No differences were found in vessel lengths taken by 3D QCA and IVUS QCA (mean difference: 0.29 ± 1.06 mm, P = 0.07). When compared with IVUS QCA, 2D QCA underestimated vessel length (mean difference: -1.78 ± 2.55, P < 0.001). Bland-Altman analysis showed close agreement and a small bias between 3D QCA and IVUS QCA in the measurement of vessel length. The vessel lumen diameter measurements by 2D QCA and 3D QCA were significantly lower than that by IVUS QCA (mean difference: -0.64 ± 0.69, P < 0.001; -0.56 ± 0.52, P < 0.001 respectively). Rotational angiography with 3D reconstruction can provide a more accurate vessel length measurement, whereas 2D and 3D QCA underestimated the vessel lumen diameter compared with IVUS QCA.

DA-9601, a standardized extract of Artemisia asiatica, blocks TNF-alpha-induced IL-8 and CCL20 production by inhibiting p38 kinase and NF-kappaB pathways in human gastric epithelial cells.

AIM: To investigate whether, or how, DA-9601, which is a new gastroprotective agent, inhibits TNF-alpha-induced inflammatory signals in gastric epithelial AGS cells. METHODS: Cell viability was determined by MTT assay. IL-8 and CCL20 promoter activities were determined by a luciferase reporter gene assay. NF-kappaB-dependent transcriptional activity was determined by I-kappaB alpha degradation, NF-kappaB p65 nuclear translocation and a luciferase activity assay. IL-8 and CCL20 gene expression and protein secretion were determined by RT-PCR and an enzyme-linked immunosorbent assay (ELISA). Total and phosphorylated forms of mitogen-activated protein kinases (MAPKs) were determined by Western blot. RESULTS: Treatment of AGS cells with DA-9601 reduced TNF-alpha-induced IL-8 and CCL20 promoter activities, as well as their gene expression and protein release. TNF-alpha also induced NF-kappaB-dependent transcriptional activity in AGS cells. In contrast, in cells treated with DA-9601, TNF-alpha-induced NF-kappaB activity was significantly blocked. Although all three MAP kinase family members were phosphorylated in response to TNF-alpha, a selective inhibitor of p38 kinase SB203580 only could inhibit both NF-kappaB-dependent transcriptional activity and IL-8 and CCL20 production, suggesting a potential link between p38 kinase and NF-kappaB-dependent pathways in AGS cells. Interestingly, DA-9601 also selectively inhibited p38 kinase phosphorylation induced by TNF-alpha. CONCLUSION: DA-9601 blocked TNF-alpha-mediated inflammatory signals by potentially modulating the p38 kinase pathway and/or a signal leading to NF-kappaB-dependent pathways in gastric epithelial cells.

Mesenchymal stem cells for tissue engineering and regenerative medicine.

Mesenchymal stem cells (MSCs) exist in bone marrow and other musculoskeletal tissues. These cells contribute to the homeostasis of musculoskeletal tissue as well as support for the growth and differentiation of primitive hemopoietic cells. Recent advancements in tissue engineering and regenerative medicine have highlighted MSCs as a potential source of cells which would differentiate to a variety of tissue tailored to individual needs. This paper briefly outlines the current status of MSCs, focusing on their biological characteristics and potential for clinical applications.

Interrelation between long-chain fatty acid oxidation rate and carnitine palmitoyltransferase 1 activity with different isoforms in rat tissues.

This study examined the interrelation between the long-chain fatty acid (LCFA) oxidation rate and the carnitine palmitoyltransferase (CPT) 1 activity in various tissues containing L-CPT1 or M-CPT1. The Liver, kidney, heart, white and red gastrocnemius muscles, and white and brown adipose tissues obtained from Sprague-Dawley rats were examined. In the tissues containing L-CPT1 the liver showed a significantly higher (P<0.01) palmitate oxidation rate and CPT1 activity than the kidney. Among the tissues containing M-CPT1, the brown adipose tissue showed the highest palmitate oxidation rate and CPT1 activity. The tissues containing M-CPT1 (r2=0.907, p<0.001) showed a strong positive correlation between the palmitate oxidation rate and the CPT1 activity. The ratios of the palmitate oxidation rate to the CPT1 activity were calculated. The ratio in the liver was highest and the ratio in the kidney was lowest among the tissues. The ratios of the tissues containing M-CPT1 were similar. These results showed that the LCFA oxidation rates in the tissues containing M-CPT1 were directly proportional to the CPT1 activity, but not similarly proportional to the CPT1 activity in the tissues containing L-CPT1. In conclusion, CPT1 activity seems very important factor for LCFA oxidation, but it might be not the only rate-limiting step in LCFA oxidation.

Spinal NF-kB activation induces COX-2 upregulation and contributes to inflammatory pain hypersensitivity.

Cyclooxygenase-2 (COX-2) is a major contributor to the elevation of spinal prostaglandin E2, which augments the processing of nociceptive stimuli following peripheral inflammation, and dynorphin has been shown to have an important role in acute and chronic pain states. Moreover, the transcription factor, nuclear factor-kappa B (NF-kB), regulates the expressions of both COX-2 and dynorphin. To elucidate the role of spinal NF-kB in the induction of inflammatory pain hypersensitivity, we examined whether activated NF-kB affects pain behavior and the expressions of the mRNAs of COX-2 and prodynorphin following peripheral inflammation. Intrathecal pretreatment with different NF-kB inhibitors, namely, NF-kB decoy or pyrrolidine dithiocarbamate, significantly reduced mechanical allodynia and thermal hyperalgesia following unilateral hindpaw inflammation evoked by complete Freund's adjuvant (CFA). These NF-kB inhibitors also suppressed the activation of spinal NF-kB and the subsequent remarkable elevation of spinal COX-2 mRNA, but not that of prodynorphin mRNA. In addition, the activation of spinal NF-kB following CFA injection was inhibited by intrathecal pretreatments with interleukin-1 beta receptor antagonist or caspase-1 inhibitor. In view of the fact that interleukin-1 beta (IL-1 beta) is the major inducer of spinal COX-2 upregulation following CFA injection, our results suggest that IL-1 beta-induced spinal COX-2 upregulation and pain hypersensitivity following peripheral inflammation are mediated through the activation of the NF-kB-associated pathways.

Effects of TNF-alpha injected intracisternally on the nociceptive jaw-opening reflex and orofacial formalin test in freely moving rats.

The present study was performed to investigate the effects of central cytokines on the modulation of nociception in the orofacial area. A nociceptive jaw-opening reflex (JOR) and an orofacial formalin test were monitored after intracisternal administration of tumor necrosis factor (TNF)-alpha in freely moving rats. Experiments were carried out on 83 male rats weighing 300-350 g and surgical procedures were performed under pentobarbital sodium. After intracisternal injection of Tnf-alpha, digastric electromyogram (dEMG) and noxious behavioral responses were monitored. In the nociceptive JOR, dEMG was not significantly changed after intracisternal injection of 200 pg and 2 ng Tnf-alpha. However, 20 ng Tnf-alpha suppressed dEMG to 72+/-6% of the control values. The orofacial formalin responses showed two distinct phases separated by a time of relative inactivity with an early short-lasting response (0-9 min, first phase) and a continuous prolonged response (10-45 min, second phase). In the inflammatory orofacial formalin test, intracisternal injection of 20 pg Tnf-alpha did not change the number of noxious behavioral responses produced by formalin injection. However, 200 pg Tnf-alpha injected intracisternally significantly increased the number of noxious behavioral responses produced by formalin injection in both the early and late phases, and 2 ng Tnf-alpha increased formalin induced noxious behavioral responses in only the late phase. A higher dose of 20 ng Tnf-alpha did not change the number of noxious behavioral responses produced by formalin injection. The hyperalgesic action of Tnf-alpha injected intracisternally was blocked by pretreatment with the interleukin-1 (IL-1) receptor antagonist. These results suggest that central Tnf-alpha modulates the transmission of nociceptive information in the orofacial area. However, the hypo/hyperalgesic response of central Tnf-alpha seems to depend on the orofacial pain model or in a dose-related manner. The hyperalgesic response of central Tnf-alpha seems to be mediated by the IL-1 receptor.

Effects of intracisternal injection of interleukin-6 on nociceptive jaw opening reflex and orofacial formalin test in freely moving rats.

The present study was performed to investigate the effects of central cytokines on the modulation of nociception in the orofacial area. To achieve this purpose, a nociceptive jaw opening reflex and an orofacial formalin test were monitored before and after intracisternal administration of interleukin-6 (IL-6) in freely moving rats. In the nociceptive jaw opening reflex, the digastric electromyogram (dEMG) was not significantly changed after intracisternal injection of 200 pg and 2 ng IL-6. However, 20 ng IL-6 suppressed dEMG to 74+/-7% of the control values. In the inflammatory orofacial formalin test, intracisternal injection of 200 pg and 2 ng IL-6 did not change the number of noxious behavioral responses produced by formalin injection. However, 20 ng IL-6 injected intracisternally significantly increased the number of noxious behavioral responses produced by formalin. The hyperalgesic action of intracisternal IL-6 in the orofacial formalin test was blocked by pretreatment with interleukin-1 (IL-1) receptor antagonist. These results suggest that IL-6 injected intracisternally modulates the transmission of nociceptive information in the orofacial area. However, the hypo/hyper-algesic response of central cytokines seems to depend on the orofacial pain model. The hyperalgesic response of central IL-6 seems to be mediated by the IL-1 receptor.