The Modulation of Phospho-Extracellular Signal-Regulated Kinase and Phospho-Protein Kinase B Signaling Pathways plus Activity of Macrophage-Stimulating Protein Contribute to the Protective Effect of Stachydrine on Acetaminophen-Induced Liver Injury.

Stachydrine, a prominent bioactive alkaloid derived from Leonurus heterophyllus, is a significant herb in traditional medicine. It has been noted for its anti-inflammatory and antioxidant characteristics. Consequently, we conducted a study of its hepatoprotective effect and the fundamental mechanisms involved in acetaminophen (APAP)-induced liver injury, utilizing a mouse model. Mice were intraperitoneally administered a hepatotoxic dose of APAP (300 mg/kg). Thirty minutes after APAP administration, mice were treated with different concentrations of stachydrine (0, 2.5, 5, and 10 mg/kg). Animals were sacrificed 16 h after APAP injection for serum and liver tissue assays. APAP overdose significantly elevated the serum alanine transferase levels, hepatic pro-inflammatory cytokines, malondialdehyde activity, phospho-extracellular signal-regulated kinase (ERK), phospho-protein kinase B (AKT), and macrophage-stimulating protein expression. Stachydrine treatment significantly decreased these parameters in mice with APAP-induced liver damage. Our results suggest that stachydrine may be a promising beneficial target in the prevention of APAP-induced liver damage through attenuation of the inflammatory response, inhibition of the ERK and AKT pathways, and expression of macrophage-stimulating proteins.

Effects of Corilagin on Lipopolysaccharide-Induced Acute Lung Injury via Regulation of NADPH Oxidase 2 and ERK/NF-κB Signaling Pathways in a Mouse Model.

Acute lung injury (ALI) and acute respiratory distress syndrome are clinically life-threatening diseases. Corilagin, a major polyphenolic compound obtained from the herb Phyllanthus urinaria, has anti-inflammatory and antioxidant properties, and in this study, we sought to evaluate the protective effects and mechanisms of corilagin on lipopolysaccharide (LPS)-induced ALI in mice. ALI was induced in the mice by the intratracheal administration of LPS, and following 30 min of LPS challenge, corilagin (5 and 10 mg/kg body weight) was administered intraperitoneally. At 6 h post-LPS administration, lung tissues were collected for analysis. Corilagin treatment significantly attenuated inflammatory cell infiltration, the production of pro-inflammatory cytokines TNF-α, IL-6, and IL-1ß, and oxidative stress in lung tissues. In addition, corilagin inhibited the LPS-induced expression of NOX2, ERK, and NF-κB. Corilagin has anti-oxidative and anti-inflammatory effects, and can effectively reduce ALI via attenuation of the NOX2 and ERK/NF-κB signaling pathways.

Polydopamine/IR820 nanoparticles as topical phototheranostics for inhibiting psoriasiform lesions through dual photothermal and photodynamic treatments.

Dual photothermal and photodynamic therapy (PTT and PDT) is an attractive approach that generates a synergistic effect for inhibiting keratinocyte hyperproliferation in the treatment of psoriasis. Here, we developed phototheranostic nanocarriers capable of producing hyperthermia and reactive oxygen species (ROS) in response to near-infrared (NIR) illumination. To this end, IR820 with photothermal and photodynamic features was embedded in nano-sized polydopamine (PDA) acting as a PTT agent. A comprehensive characterization of the PDA/IR820 nanosystem was performed according to its morphology, size, zeta potential, UV absorbance, and heat generation. Its therapeutic efficacy was assessed by a keratinocyte-based study and using an imiquimod (IMQ)-stimulated psoriasiform murine model. PDA/IR820 nanoparticles were facilely internalized into keratinocytes and mainly resided in lysosomes. Upon irradiation with NIR light, ROS were generated inside the keratinocytes to cause a photodynamic effect. The live/dead cell assay and cytotoxicity assay demonstrated that PDA and IR820 acted as effective photoabsorbers to induce keratinocyte death. The highest cytotoxic effect was detected in the group of NIR-irradiated PDA/IR820 nanoparticles, which killed 52% of keratinocytes. The nanosystem acted through the caspase and poly ADP-ribose polymerase (PARP) pathways to induce keratinocyte apoptosis. In vitro and in vivo skin permeation indicated the selective accumulation of the topically applied PDA/IR820 nanoparticles within psoriasiform skin, suggesting their skin-targeting capability. The combination of PDA/IR820 nanoparticles and NIR irradiation increased the skin temperature by 11.7 °C. PTT/PDT eliminated psoriasiform plaques in mice by decreasing hyperplasia, inhibiting cytokine overexpression, and recovering the barrier function. The epidermal thickness of the IMQ-treated skin was reduced from 134 to 34 µm by the nanocarriers plus NIR. The IR820 nanoparticles were largely deposited on the inflamed areas of psoriasiform lesions for monitoring the severity of inflammation. The image-guided phototheranostic nanoparticles showed their potential for applications in psoriasis management via noninvasive topical administration.

Investigation of Cerebrospinal Fluid Electrolytes and Acid-Base Expressions in Asian Adults.

BACKGROUND: In previous literature, reference values for cerebrospinal fluid (CSF) may be based on patients who were not truly healthy, other species, or outdated information. In the present study, we performed a lumbar puncture in patients requiring spinal anesthesia by a reasonable indication to evaluate CSF parameters in healthy adults. METHODS: All patients between the ages of 20 and 70 years scheduled for elective orthopedic or urologic surgery requiring spinal anesthesia were enrolled in this study. We measured electrolytes and gas tension analysis in CSF and whole blood samples in adult humans. RESULTS: A total of 28 patients were included with an average age of 44.2 years. The concentration of Na^+ in blood was slightly lower when compared with that in CSF. There were significantly higher levels of K^+ and Ca^(2+) in the blood when we compared with CSF. Significantly lower levels of Cl^- and Mg^(2+) in the blood were observed when compared with CSF. The glucose level of CSF was about half of that in blood. CONCLUSIONS: We provided updated reference values for various solutes in blood and CSF in adults. Analysis of CSF parameters and relevant paired blood samples is highly informative, helping clinicians diagnose a variety of central nervous system diseases.

Cerebrospinal fluid electrolytes and acid-base in diabetic patients.

BACKGROUND: Diabetes mellitus (DM) has detrimental effects on the function of microvascular beds, resulting in blood-brain barrier (BBB) dysfunction. The objective of the study was to investigate whether DM affects the brain physiology through composition of cerebrospinal fluid (CSF) and compare gas tension and electrolyte levels in CSF between the diabetic and nondiabetic populations. METHODS: Patients aged between 20 and 70 years scheduled for elective orthopedic or urologic surgery requiring spinal anesthesia were enrolled. They were assigned to either of the two groups (control or type 2 DM). Gas tension and electrolytes in the CSF and whole blood samples were measured in both groups. RESULTS: All 49 enrolled patients (24 in the control and 25 in the DM group) completed the study. The concentrations of Na+ and Mg2+ in the blood were significantly lower in the DM group than those in the control. The levels of pCO2 and HCO 3 - in the CSF were lower in the DM group than in the control group. In addition, there was a marked increase in the glucose level in both the blood and CSF in the DM group. CONCLUSION: The results show that there were some homeostatic changes in blood and CSF in patients with DM.

Increased FIO2 influences SvO2 interpretation and accuracy of Fick-based cardiac output assessment in cardiac surgery patients: A prospective randomized study.

INTRODUCTION: The study aimed to reveal how the fraction of inspired oxygen (FIO2) affected the value of mixed venous oxygen saturation (SvO2) and the accuracy of Fick-equation-based cardiac output (Fick-CO). METHODS: Forty two adult patients who underwent elective cardiac surgery were enrolled and randomly divided into 2 groups: FIO2 < 0.7 or >0.85. Under stable general anesthesia, thermodilution-derived cardiac output (TD-CO), SvO2, venous partial pressure of oxygen, hemoglobin, arterial oxygen saturation, arterial partial pressure of oxygen, and blood pH levels were recorded before surgical incision. RESULTS: Significant differences in FIO2 values were observed between the 2 groups (0.56 ±â€Š0.08 in the <70% group and 0.92 ±â€Š0.03 in the >0.85 group; P < .001). The increasing FIO2 values lead to increases in SvO2, venous partial pressure of oxygen, and arterial partial pressure of oxygen, with little effects on cardiac output and hemoglobin levels. When comparing to TD-CO, the calculated Fick-CO in both groups had moderate Pearson correlations and similar linear regression results. Although the FIO2 <0.7 group presented a less mean bias and a smaller limits of agreement, neither group met the percentage error criteria of <30% in Bland-Altman analysis. CONCLUSION: Increased FIO2 may influence the interpretation of SvO2 and the exacerbation of Fick-CO estimation, which could affect clinical management. TRIAL REGISTRATION: ClinicalTrials.gov ID number: NCT04265924, retrospectively registered (Date of registration: February 9, 2020).

Corilagin reduces acetaminophen-induced hepatotoxicity through MAPK and NF-κB signaling pathway in a mouse model.

Corilagin is a major active polyphenolic tannins extracted from Phyllanthus urinaria, an important herb used in traditional medicine. Previous reports demonstrated that corilagin possesses antioxidant and anti-inflammatory properties. Therefore, this study aimed to evaluate its hepatoprotective effects and mechanisms on acetaminophen (APAP)-induced liver injury in mice. Mice included in this study were intraperitoneally injected with a hepatotoxic APAP dose (300 mg/kg). After a 30 min of APAP administration, corilagin was injected intraperitoneally at concentrations of 0, 1, 5, 10, and 20 mg/kg. Then, after 16 h of corilagin treatment, mice were sacrificed for further analysis. APAP overdose significantly elevated the serum ALT level, hepatic myeloperoxidase (MPO) activity, cytokines (TNF-α, IL-1ß, and IL-6) production, malondialdehyde (MDA) activity, and ERK/JNK MAPK and NF-κB protein expressions. Corilagin treatment significantly decreased these parameters in a dose-dependent manner (1-20 mg/kg). This study demonstrated that corilagin may be a potential therapeutic target for the prevention of APAP-induced hepatotoxicity by down-regulating the inflammatory response and by inhibiting ERK/JNK MAPK and NF-κB signaling pathways.

Esculetin Ameliorates Lipopolysaccharide-Induced Acute Lung Injury in Mice Via Modulation of the AKT/ERK/NF-κB and RORγt/IL-17 Pathways.

Esculetin, a coumarin derivative from various natural plants, has an anti-inflammatory property. In the present study, we examined if esculetin has any salutary effects against lipopolysaccharide (LPS)-induced acute lung injury (ALI) in mice. Acute lung injury (ALI) was induced via the intratracheal administration of LPS, and esculetin (20 and 40 mg/kg) was given intraperitoneally 30 min before LPS challenge. After 6 h of LPS administration, lung tissues were collected for analysis. Pretreatment with esculetin significantly attenuated histopathological changes, inflammatory cell infiltration, and production of pro-inflammatory cytokines, such as tumor necrosis factor (TNF)-α, interleukin (IL)-1ß, and IL-6, in the lung tissue. Furthermore, esculetin inhibited the protein kinase B (AKT), extracellular signal-regulated kinase (ERK), and nuclear factor-kappa B (NF-κB) pathways and downregulated the expression of RORγt and IL-17 in LPS-induced ALI. Our results indicated that esculetin possesses anti-inflammatory and protective effects against LPS-induced ALI via inhibition of the AKT/ERK/NF-κB and RORγt/IL-17 pathways.

The MAP2K4/JNK/c-Jun Signaling Pathway Plays A Key Role In Dexmedetomidine Protection Against Acetaminophen-Induced Liver Toxicity.

PURPOSE: Dexmedetomidine [DEX; (S)-4-[1-(2,3-dimethylphenyl)ethyl]-3H-imidazole] is a selective α2-adrenergic receptor (α2-AR) agonist that attenuates the liver damage associated with local or systemic inflammation. However, it remains unclear whether DEX has protective effects against acetaminophen (Paracetamol, PARA)-induced liver toxicity (PILT). METHODS: PILT mice were established by intraperitoneal administration of a hepatotoxic dose of acetaminophen (300 mg/kg). Thirty minutes later, the mice were treated with DEX at a concentration of 0, 5, 25, or 50 µg/kg. Blood and liver samples were obtained for further analysis. RESULTS: DEX treatment significantly attenuated PILT in mice, with the strongest beneficial effects at a dose of 25 µg/kg. The levels of hepatic cytokines, tumor necrosis factor-alpha (TNF-α) and interleukin-6 (IL-6), in addition to myeloperoxidase (MPO) activity, were significantly decreased following DEX treatment. Moreover, DEX treatment reduced macrophage recruitment around the area of hepatotoxicity and the expression levels of hepatic phosphorylated mitogen-activated protein kinase kinase 4 (MAP2K4), c-jun N-terminal kinase (JNK), and c-Jun expression induced by acetaminophen overdose. CONCLUSION: The data suggest that DEX likely downregulates the JNK signaling pathway and its downstream effectors to promote its hepatoprotective effect, providing a clinical application of DEX for the attenuation of PILT.

Preoperative Right Ventricular Dysfunction Indicates High Vasoactive Support Needed After Cardiac Surgery.

OBJECTIVE: The aim of this study was to explore the relationship between preoperative right ventricular (RV) function and high vasoactive-inotropic score (VIS) after cardiac surgery. DESIGN: Prospective observational study. SETTING: A single medical center setting. PARTICIPANTS: One hundred three patients undergoing elective cardiac surgery. INTERVENTIONS: None. MEASUREMENTS AND MAIN RESULTS: Consecutive patients referred for cardiac surgery were enrolled prospectively. Comprehensive transesophageal echocardiography was performed before sternal incision. Specific RV indices, encompassing RV fractional area change, tricuspid annular plane systolic excursion, and RV global longitudinal strain (RVGLS), were measured offline. High VIS was defined as a maximum VIS of ≥20 in 24 hours postoperatively. Postoperative adverse events were recorded. One hundred three patients (mean age 61.2 ± 11.0, 72 men) were included in this study, where 17 patients (16.5%) achieved high VIS with a mean maximum VIS of 39 in 24 hours postoperatively. Patients with high VIS encountered increased occurrence of extracorporeal membrane oxygenation placement, acute kidney injury, and mortality. Risk factors for high VIS included operation type, cardiopulmonary bypass duration, left atrium size, and pre-incisional RV indices. After adjustment for age, left ventricular ejection fraction, and the covariates, only RVGLS (odds ratio 1.19, p = 0.011) showed an independent association with high VIS. The optimal cutoff of RVGLS was -16.7% (sensitivity of 88.2%, specificity of 75.6%). CONCLUSION: Preoperative RV dysfunction is an independent risk factor for postoperative high VIS. Pre-incisional RVGLS is a reliable tool to predict high VIS after cardiac surgery. Patients with high VIS had increased adverse events postoperatively.

IL-17 deficiency attenuates acetaminophen-induced hepatotoxicity in mice.

Acetaminophen (APAP) overdose results in the production of reactive oxygen species (ROS), hepatocyte necrosis, and cell death, and leads to acute liver failure. Interleukin-17 (IL-17), a pro-inflammatory cytokine, plays a key role in the recruitment of neutrophils into sites of inflammation and subsequent damage after liver ischemia-reperfusion injury. In this study, we employed IL-17 knockout (KO) mice to investigate the role of IL-17 in APAP-induced hepatotoxicity. IL-17 wide type (WT) and IL-17 KO mice received an intraperitoneal injection of APAP (300 mg/kg). After 16 h of treatment, the hepatic injury, inflammatory mediators, immune cell infiltration, and western blotting were examined and analyzed. The serum alanine transferase (ALT) enzyme levels and hepatic myeloperoxidase (MPO) activity were significantly elevated 16 h after APAP treatment in the WT mice. IL-17 deficiency significantly attenuates APAP-induced liver injury, MPO activity, pro-inflammatory cytokines (tumor necrosis factor-α, IL-6 and interferon-γ) levels and inflammatory cell (neutrophils, macrophage) infiltration in the liver. Moreover, phosphorylated extracellular signal-regulated kinase (ERK) was significantly decreased at 16 h after APAP treatment in the IL-17 KO mice compared with the IL-17 WT mice. Our data suggests that IL-17 plays a pivotal role in APAP-induced hepatotoxicity through modulation of inflammatory response, and perhaps in part through the ERK signaling pathway. Blockade of IL-17 could be a potential therapeutic target for APAP-induced hepatotoxicity.

Video laryngoscopy-assisted tracheal intubation in airway management.

INTRODUCTION: Video laryngoscopy-assisted tracheal intubation devices have become alternatives to traditional laryngoscopes in recent years. This review will provide information on commonly used video laryngoscopes and their clinical applications in airway management. AREAS COVERED: In this review, the differences between video laryngoscopy and direct laryngoscopy, and the utilization of video laryngoscopes in specific clinical settings are discussed. EXPERT COMMENTARY: Video laryngoscopy should be embraced as an initial approach to intubation in patients with suspected difficult airway. Acute care providers should be familiar with more than one intubation techniques so that a rescue attempt can be applied promptly. Continual practice and familiarity with new video laryngoscopes are still essential to maximize the effectiveness and minimize the complications of using these devices.

Comparison of right ventricular measurements by perioperative transesophageal echocardiography as a predictor of hemodynamic instability following cardiac surgery.

BACKGROUND: The relationship between perioperative right ventricular (RV) performance and hemodynamic instability after cardiac surgery seemed less portrayed. Therefore, we sought to elucidate this relationship and compare the accuracy of different RV systolic indices in predicting outcome of cardiac surgery. METHODS: This study enrolled consecutive patients referred for cardiac surgeries. Exclusion criteria were non-sinus rhythm or contraindications to transesophageal echocardiography (TEE). TEE exam and simultaneous pulmonary hemodynamics were recorded in two stages: after induction of anesthesia and before sternotomy (stage 1), and after sternal closure (stage 2). RV measurements performed offline included fractional area change (RVFAC), tricuspid annular plane systolic excursion (TAPSE), peak systolic tricuspid annular velocity (RVS'), myocardial performance index (RVMPI), and global longitudinal strain (RVGLS). The end point was defined as prolonged use (>24 h) of postoperative inotropic agent in the intensive care unit (ICU). RESULTS: The study population included 68 patients (mean age 61 ± 11 y; 49 men). Twenty-two of these patients (32%) were administered inotropic agents for a prolonged period with a mean duration of 63.9 ± 5.3 h, accompanied with significantly longer ventilator use (p = 0.006) and longer ICU stay (p = 0.001) than patients without a prolonged inotropic agent use. Multivariable analysis demonstrated that only RVGLS in either stage 1 (odds ratio [OR] 1.11, p = 0.048) or stage 2 (OR 1.15, p = 0.018) was significantly associated with the outcome, especially a RVGLS > -13.5% in stage 2 demonstrating high risk of prolonged inotropic agent use after cardiac surgery (OR 7.37, p = 0.016). CONCLUSION: RVGLSs performed using perioperative TEE are reliably associated with hemodynamic instability following cardiac surgery. This finding adds substantial information to postoperative critical care.

C-C Chemokine Ligand-5 is critical for facilitating macrophage infiltration in the early phase of liver ischemia/reperfusion injury.

CCL5/RANTES, a chemoattractant for myeloid cells, is induced by hepatic ischemia/reperfusion injury (IRI). The roles of CCL5 in hepatic IRI were carried out by means of CCL5 immunodepletion, antagonistic competition by Met-CCL5, and treatment with recombinant murine CCL5 (rmCCL5). Depletion or inhibition of CCL5 reduced severity of hepatic IRI, whereas rmCCL5 treatment aggravated liver IRI as manifested in elevated serum alanine aminotransferase (ALT) and tissue myeloperoxidase (MPO) levels. Moreover, IRI severity was reduced in CCL5-knockout (CCL5-KO) mice versus wildtype (WT) mice, with drops in serum ALT level, intrahepatic MPO activity, and histological pathology. Bone marrow transplantion (BMT) studies show that myeloid cells and tissue cells are both required for CCL5-aggravated hepatic IRI. The profile of liver-infiltrating leukocyte subsets after hepatic reperfusion identified CD11b+ cells as the only compartment significantly reduced in CCL5-KO mice versus WT controls at early reperfusion phase. The role of CCL5 recruiting CD11b+ cells in early reperfusion was validated by in vitro transwell migration assay of murine primary macrophages (broadly characterized by their CD11b expression) in response to liver lysates after early reperfusion. Taken together, our results demonstrate a sequence of early events elicited by CCL5 chemoattracting macrophage that result in inflammatory aggravation of hepatic IRI.

ERK Signaling Pathway Plays a Key Role in Baicalin Protection Against Acetaminophen-Induced Liver Injury.

Acetaminophen (APAP) overdose causes hepatocytes necrosis and acute liver failure. Baicalin (BA), a major flavonoid of Scutellariae radix, has potent hepatoprotective properties in traditional medicine. In the present study, we investigated the protective effects of BA on a APAP-induced liver injury in a mouse model. The mice received an intraperitoneal hepatotoxic dose of APAP (300[Formula: see text]mg/kg) and after 30[Formula: see text]min, were treated with BA at concentrations of 0, 15, 30, or 60[Formula: see text]mg/kg. After 16[Formula: see text]h of treatment, the mice were sacrificed for further analysis. APAP administration significantly elevated the serum alanine transferase (ALT) enzyme levels and hepatic myeloperoxidase (MPO) activity when compared with control animals. Baicalin treatment significantly attenuated the elevation of liver ALT levels, as well as hepatic MPO activity in a dose- dependent manner (15-60[Formula: see text]mg/kg) in APAP-treated mice. The strongest beneficial effects of BA were seen at a dose of 30[Formula: see text]mg/kg. BA treatment at 30[Formula: see text]mg/kg after APAP overdose reduced elevated hepatic cytokine (TNF-[Formula: see text] and IL-6) levels, and macrophage recruitment around the area of hepatotoxicity in immunohistochemical staining. Significantly, BA treatment can also decrease hepatic phosphorylated extracellular signal-regulated kinase (ERK) expression, which is induced by APAP overdose. Our data suggests that baicalin treatment can effectively attenuate APAP-induced liver injury by down-regulating the ERK signaling pathway and its downstream effectors of inflammatory responses. These results support that baicalin is a potential hepatoprotective agent.

Baicalin Attenuates IL-17-Mediated Acetaminophen-Induced Liver Injury in a Mouse Model.

BACKGROUND: IL-17 has been shown to be involved in liver inflammatory disorders in both mice and humans. Baicalin (BA), a major compound extracted from traditional herb medicine (Scutellariae radix), has potent hepatoprotective properties. Previous study showed that BA inhibits IL-17-mediated lymphocyte adhesion and downregulates joint inflammation. The aim of this study is to investigate the role of IL-17 in the hepatoprotective effects of BA in an acetaminophen (APAP)-induced liver injury mouse model. METHODS: Eight weeks male C57BL/6 (B6) mice were used for this study. Mice received intraperitoneal hepatotoxic injection of APAP (300 mg/kg) and after 30 min of injection, the mice were treated with BA at a concentration of 30 mg/kg. After 16 h of treatment, mice were killed. Blood samples and liver tissues were harvested for analysis of liver injury parameters. RESULTS: APAP overdose significantly increased the serum alanine transferase (ALT) levels, hepatic activities of myeloperoxidase (MPO), expression of cytokines (TNF-α, IL-6, and IL-17), and malondialdehyde (MDA) activity when compared with the control animals. BA treatment after APAP administration significantly attenuated the elevation of these parameters in APAP-induced liver injury mice. Furthermore, BA treatment could also decrease hepatic IL-17-producing γδT cells recruitment, which was induced after APAP overdose. CONCLUSION: Our data suggested that baicalin treatment could effectively decrease APAP-induced liver injury in part through attenuation of hepatic IL-17 expression. These results indicate that baicalin is a potential hepatoprotective agent.

The Effects of Volume-Controlled and Pressure-Controlled Ventilation on Lung Mechanics, Oxidative Stress, and Recovery in Gynecologic Laparoscopic Surgery.

STUDY OBJECTIVE: To compare ventilation variables, changes in oxidative stress, and the quality of recovery in 2 different ventilation strategies (volume-controlled ventilation [VCV] and pressure-controlled ventilation [PCV]) during gynecologic laparoscopic surgery. DESIGN: A prospective randomized controlled trial (Canadian Task Force classification I). SETTING: One university teaching hospital in Taiwan. PATIENTS: Women scheduled for laparoscopic gynecologic surgery. INTERVENTIONS: Women were randomly assigned to receive either VCV or PCV during surgery. MEASUREMENTS AND MAIN RESULTS: Ventilation variables were recorded 1 minute before and 1 hour after pneumoperitoneum. Blood samples were collected for malondialdehyde measurement at 7 points: 1 minute before and 1 hour after pneumoperitoneum; 30, 60, 90, and 120 minutes after deflation; and 24 hours after surgery. Postoperative recovery was assessed by using a 9-item quality of recovery score at 24 hours after surgery. A total of 52 women randomly allocated to the VCV (n = 27) or PCV (n = 25) group completed the study. We found that after 1 hour of insufflation the PCV group had lower peak airway pressure (22.0 ± 3.4 vs 26.6 ± 4.1 cm H2O, p < .0001) and higher compliance (28.4 ± 3.7 vs 24.1 ± 3.3 mL/cm H2O, p < .0001) than the VCV group. In plasma levels of malondialdehyde, there were no significant differences between the 2 groups at 7 time points. The levels significantly increased in both groups after 1 hour of pneumoperitoneum and peaked at 2 hours after deflation. During postoperative recovery, lower scores were obtained at 24 hours after surgery compared with preoperative scores, but there were no significant differences between the 2 groups. CONCLUSION: PCV is an alternative ventilation mode in gynecologic laparoscopic surgery. However, PCV offered lower peak airway pressure and higher compliance than VCV but no advantages over VCV in oxidative stress or quality of recovery.

A comparison of parecoxib and thoracic epidural analgesia for postoperative analgesia following Nuss procedure.

BACKGROUND: The purpose of this study was to compare the results of thoracic epidural analgesia (TEA) and parecoxib in controlling postoperative pain after the Nuss procedure. METHODS: Between August 2005 and July 2014, 120 adolescents and adults underwent Nuss procedures and received either TEA or parecoxib for postoperative pain control. Demographic data, preoperative preparation times, visual analog scale (VAS) pain scores from postoperative day 1 to day 5, medical costs of pain control, days to Foley catheter removal, days to being able to sit up, days to being able to walk, days of hospital stay, nausea/vomiting scores, and complications related to pain control were compared. RESULTS: A total of 106 patients received TEA, and 14 received parecoxib. No between-group differences in demographics were observed. Patients in the parecoxib group had shorter preparation times (p<0.001), lower VAS pain scores from postoperative day 2 to day 5 (day 2, p=0.006; day 3, p=0.006; day 4, p<0.001; day 5, p<0.001), shorter hospital stays (p<0.001), lower pain control costs (p<0.001), and lower nausea/vomiting scores (p=0.046). CONCLUSIONS: For adolescents and adults undergoing the Nuss procedure, parecoxib affords better pain control efficacy, a shorter hospital stay, lower medical pain control costs, and fewer side effects compared with TEA.

Lack of interleukin-17 leads to a modulated micro-environment and amelioration of mechanical hypersensitivity after peripheral nerve injury in mice.

Interleukin-17 (IL-17) is involved in a wide range of inflammatory disorders and in recruitment of inflammatory cells to injury sites. A recent study of IL-17 knock-out mice revealed that IL-17 contributes to neuroinflammation and neuropathic pain after peripheral nerve injury. Surprisingly, little is known of micro-environment modulation by IL-17 in injured sites and in pathologically related neuroinflammation and chronic neuropathic pain. Therefore, we investigated nociceptive sensitization, immune cell infiltration, myeloperoxidase (MPO) activity, and expression of multiple cytokines and opioid peptides in damaged nerves of wild-type (IL-17(+/+)) and IL-17 knock-out (IL-17(-/-)) mice after partial sciatic nerve ligation. Our results demonstrated that the IL-17(-/-) mice had less behavioral hypersensitivity after partial sciatic nerve ligation, and inflammatory cell infiltration and pro-inflammatory cytokine (tumor necrosis factor-α, IL-6, and interferon-γ) levels in damaged nerves were significantly decreased, with the levels of anti-inflammatory cytokines IL-10 and IL-13, and expressions of enkephalin, ß-endorphin, and dynorphin were also decreased compared to those in wild-type control mice. In conclusion, we provided evidence that IL-17 modulates the micro-environment at the level of the peripheral injured nerve site and regulates progression of behavioral hypersensitivity in a murine chronic neuropathic pain model. The attenuated behavioral hypersensitivity in IL-17(-/-) mice could be a result of decreased inflammatory cell infiltration to the injured site, resulting in modulation of the pro- and anti-inflammatory cytokine milieu within the injured nerve. Therefore, IL-17 may be a critical component for neuropathic pain pathogenesis and a novel target for therapeutic intervention for this and other chronic pain states.