Burns ; complications ; metabolism ; Humans ; Inflammation ; etiology ; metabolism ; prevention & control

Bronchopulmonary Dysplasia ; etiology ; pathology ; prevention & control ; Humans ; Infant, Newborn ; Infant, Premature ; Inflammation ; complications ; Lung ; pathology ; Respiration, Artificial ; adverse effects

The inflammation factors and roles of them in acute coronary syndrome (ACS) were explored. The similarity between the theory of pathogenic toxin in Chinese Medicine and the inflammation response theory in ACS was discussed. The exploration of new inflammatory factors may be helpful for Chinese Medicine in the research of ACS.
Acute Coronary Syndrome ; complications ; diagnosis ; prevention & control ; therapy ; Humans ; Inflammation ; complications ; etiology ; pathology ; therapy ; Inflammation Mediators ; physiology ; Medicine, Chinese Traditional ; Prognosis ; Toxins, Biological ; adverse effects

Alzheimer Disease ; etiology ; prevention & control ; Cytokines ; physiology ; Humans ; Inflammation ; complications ; Interleukin-1 ; physiology ; Nerve Growth Factors ; Risk Factors ; S100 Calcium Binding Protein beta Subunit ; S100 Proteins ; physiology

OBJECTIVEAnesthetic isoflurane plus surgery has been reported to induce cognitive impairment. The underlying mechanism and targeted intervention remain largely to be determined. Ginsenoside Rb1 was reported to be neuroprotective. We therefore set out to determine whether ginsenoside Rb1 can attenuate isoflurane/surgery-induced cognitive dysfunction via inhibiting neuroinflammation and oxidative stress.

METHODSFive-months-old C57BL/6J female mice were treated with 1.4% isoflurane plus abdominal surgery for two hours. Sixty mg/kg ginsenoside Rb1 were given intraperitoneally from 7 days before surgery. Cognition of the mice were assessed by Barnes Maze. Levels of postsynaptic density-95 and synaptophysin in mice hippocampus were measured by Western blot. Levels of reactive oxygen species, tumor necrosis factor-α and interleukin-6 in mice hippocampus were measured by ELISA.

RESULTSHere we show for the first time that the ginsenoside Rb1 treatment attenuated the isoflurane/surgery-induced cognitive impairment. Moreover, ginsenoside Rb1 attenuated the isoflurane/surgery-induced synapse dysfunction. Finally, ginsenoside Rb1 mitigated the isoflurane/surgery-induced elevation levels of reactive oxygen species, tumor necrosis factor-α and interleukin-6 in the mice hippocampus.

CONCLUSIONThese results suggest that ginsenoside Rb1 may attenuate the isoflurane/surgery-induced cognitive impairment by inhibiting neuroinflammation and oxidative stress pending future studies.

Anesthetics, Inhalation ; adverse effects ; Animals ; Cognition ; Cognitive Dysfunction ; etiology ; prevention & control ; Female ; Ginsenosides ; pharmacology ; Hippocampus ; drug effects ; Inflammation ; etiology ; prevention & control ; Isoflurane ; adverse effects ; Medicine, Chinese Traditional ; Mice ; Mice, Inbred C57BL ; Oxidative Stress ; Postoperative Complications ; etiology ; prevention & control ; Random Allocation ; Surgical Procedures, Operative ; adverse effects ; Synapses ; metabolism

Investigation of pain requires measurements of nociceptive sensitivity and other pain-related behaviors. Recent studies have indicated the superiority of gait analysis over traditional evaluations (e.g., skin sensitivity and sciatic function index [SFI]) in detecting subtle improvements and deteriorations in animal models. Here, pain-related gait parameters, whose criteria include (1) alteration in pain models, (2) correlation with nociceptive threshold, and (3) normalization by analgesics, were identified in representative models of neuropathic pain (spared nerve injury: coordination data) and inflammatory pain (intraplantar complete Freund's adjuvant: both coordination and intensity data) in the DigiGait™ and CatWalk™ systems. DigiGait™ had advantages in fixed speed (controlled by treadmill) and dynamic SFI, while CatWalk™ excelled in intrinsic velocity, intensity data, and high-quality 3D images. Insights into the applicability of each system may provide guidance for selecting the appropriate gait imaging system for different animal models and optimization for future pain research.
Analgesics ; administration & dosage ; Animals ; Freund's Adjuvant ; administration & dosage ; Gait ; drug effects ; Gait Analysis ; methods ; Image Processing, Computer-Assisted ; Inflammation ; chemically induced ; Male ; Neuralgia ; physiopathology ; prevention & control ; Pain ; etiology ; physiopathology ; prevention & control ; Rats, Sprague-Dawley

PURPOSE: Oxidative stress during CO2 pneumoperitoneum is reported to be associated with decreased bioactivity of nitric oxide (NO). However, the changes in endothelial nitric oxide synthase (eNOS), inducible nitric oxide synthase (iNOS), and arginase during CO2 pneumoperitoneum have not been elucidated. MATERIALS AND METHODS: Thirty male Sprague-Dawley rats were randomized into three groups. After anesthesia induction, the abdominal cavities of the rats of groups intra-abdominal pressure (IAP)-10 and IAP-20 were insufflated with CO2 at pressures of 10 mm Hg and 20 mm Hg, respectively, for 2 hours. The rats of group IAP-0 were not insufflated. After deflation, plasma NO was measured, while protein expression levels and activity of eNOS, iNOS, arginase (Arg) I, and Arg II were analyzed with aorta and lung tissue samples. RESULTS: Plasma nitrite concentration and eNOS expression were significantly suppressed in groups IAP-10 and IAP-20 compared to IAP-0. While expression of iNOS and Arg I were comparable between the three groups, Arg II expression was significantly greater in group IAP-20 than in group IAP-0. Activity of eNOS was significantly lower in groups IAP-10 and IAP-20 than in group IAP-0, while iNOS activity was significantly greater in group IAP-20 than in groups IAP-0 and IAP-10. Arginase activity was significantly greater in group IAP-20 than in groups IAP-0 and IAP-10. CONCLUSION: The activity of eNOS decreases during CO2 pneumoperitoneum, while iNOS activity is significantly increased, a change that contributes to increased oxidative stress and inflammation. Moreover, arginase expression and activity is increased during CO2 pneumoperitoneum, which seems to act inversely to the NO system.
Animals ; Aorta/*physiology ; Arginase/*antagonists & inhibitors ; Enzyme Inhibitors/administration & dosage/pharmacology ; Inflammation/etiology/*prevention & control ; Injections, Subcutaneous ; Lung Injury/etiology/prevention & control ; Male ; Nitric Oxide/metabolism ; Nitric Oxide Synthase Type II/*metabolism ; Nitric Oxide Synthase Type III/*metabolism ; Oxidative Stress/*drug effects ; Pneumoperitoneum/*complications/drug therapy ; Rats ; Rats, Sprague-Dawley

OBJECTIVETo evaluating the effect of different levels of blood glucose control on inflammatory response and prognosis of the patients in surgical intensive care unit (SICU).

METHODSOne hundred and eighty-eight patients admitted to SICU were randomly divided into three groups, blood glucose were controlled by insulin infusion. Group A (75 cases): the mean blood glucose (MBG) was maintained at the level of 4.4 - 6.1 mmol/L. Group B (75 cases): MBG was maintained at the level of 6.7 - 8.3 mmol/L. Group C (38 cases): MBG was maintained at the level of 10.0 - 11.1 mmol/L. Blood glucose control was achieved with an effected computerized protocol. The outcome was evaluated by days in ICU, days to wean mechanical ventilation, infection, amount of red blood cell transfusion, hospital mortality and ICU cost.

RESULTSCompared with other groups, hypoglycemia (< 3.3 mmol/L) in Group A was significantly increased (P < 0.05). Compared with Group C, red blood cell transfusion and infection were significantly reduced in Group A and Group B (P < 0.05). Compared with Group C, days of mechanical ventilation and days in ICU in Group A were significantly reduced (P < 0.05). Hospital mortality and ICU cost were reduced in Group A compared with the other groups (P > 0.05).

CONCLUSIONSTo maintain blood glucose in normal range with intensive insulin therapy has potential positive impact on SICU patients' outcome and can reduce days in ICU and ICU cost. Further correlation research is needed to determine the best levels of blood glucose in ICU patients.

Adolescent ; Adult ; Aged ; Aged, 80 and over ; Blood Glucose ; metabolism ; Critical Illness ; Female ; Humans ; Hypoglycemic Agents ; administration & dosage ; therapeutic use ; Inflammation ; blood ; etiology ; prevention & control ; Insulin ; administration & dosage ; therapeutic use ; Insulin Infusion Systems ; Intensive Care Units ; Male ; Middle Aged ; Postoperative Care ; methods ; Postoperative Complications ; blood ; etiology ; prevention & control ; Prognosis ; Treatment Outcome

OBJECTIVETo investigate the effect of H₂S on lower limb ischemia-reperfusion (LIR) induced lung injury and explore the underlying mechanism.

METHODSWistar rats were randomly divided into control group, IR group, IR+ Sodium Hydrosulphide (NaHS) group and IR+ DL-propargylglycine (PPG) group. IR group as lung injury model induced by LIR were given 4 h reperfusion following 4 h ischemia of bilateral hindlimbs with rubber bands. NaHS (0.78 mg/kg) as exogenous H₂S donor and PPG (60 mg/kg) which can suppress endogenous H₂S production were administrated before LIR, respectively. The lungs were removed for histologic analysis, the determination of wet-to-dry weight ratios and the measurement of mRNA and protein levels of aquaporin-1 (AQP₁), aquaporin-5 (AQP₅) as indexes of water transport abnormality, and mRNA and protein levels of Toll-like receptor 4 (TLR₄), myeloid differentiation primary-response gene 88 (MyD88) and p-NF-κB as indexes of inflammation.

RESULTSLIR induced lung injury was accompanied with upregulation of TLR₄-Myd88-NF-κB pathway and downregulation of AQP1/AQP₅. NaHS pre-treatment reduced lung injury with increasing AQP₁/AQP₅ expression and inhibition of TLR₄-Myd88-NF-κB pathway, but PPG adjusted AQP₁/AQP₅ and TLR4 pathway to the opposite side and exacerbated lung injury.

CONCLUSIONEndogenous H₂S, TLR₄-Myd88-NF-κB pathway and AQP₁/AQP₅ were involved in LIR induced lung injury. Increased H₂S would alleviate lung injury and the effect is at least partially depend on the adjustment of TLR₄-Myd88-NF-κB pathway and AQP₁/AQP₅ expression to reduce inflammatory reaction and lessen pulmonary edema.

Acute Lung Injury ; complications ; pathology ; prevention & control ; Animals ; Aquaporins ; metabolism ; Drug Evaluation, Preclinical ; Edema ; etiology ; pathology ; Hydrogen Sulfide ; pharmacology ; therapeutic use ; Inflammation ; prevention & control ; Lung ; pathology ; Male ; Myeloid Differentiation Factor 88 ; metabolism ; NF-kappa B ; metabolism ; Random Allocation ; Rats ; Rats, Wistar ; Reperfusion Injury ; complications ; pathology ; prevention & control ; Toll-Like Receptor 4 ; metabolism ; Water ; metabolism

At present ventricular remodeling (VR) is regarded as the main pathological basis of chronic heart failure after acute myocardial infarction (AMI), and preventing VR after AMI is of great importance for the prevention of heart failure. Previously, it has not been paid enough attention to the role of inflammation and autoimmune injury during the process of VR after AMI. This topic was discussed in the paper and the treating strategies with Chinese and Western medicine were also explored.
Animals ; Anti-Inflammatory Agents ; therapeutic use ; Drug Therapy, Combination ; Drugs, Chinese Herbal ; therapeutic use ; Heart Failure ; prevention & control ; Humans ; Inflammation ; drug therapy ; etiology ; immunology ; Myocardial Infarction ; complications ; physiopathology ; Prednisone ; therapeutic use ; Ventricular Remodeling ; drug effects