Search

We aimed to investigate whether the cardioprotection of sevoflurane against ischemia-reperfusion (IR) injury is via inhibiting endoplasmic reticulum stress. The rat in vivo model of myocardial IR injury was induced by ligation of the left anterior descending coronary artery. Sevoflurane significantly ameliorated the reduced cardiac function, increased infarct size, and elevated troponin I level and lactate dehydrogenase activity in plasma induced by IR injury. Sevoflurane suppressed the IR-induced myocardial apoptosis. The increased protein levels of glucose-regulated protein 78 and C/EBP homologous protein (CHOP) after myocardial IR were significantly reduced by sevoflurane. The protein levels of phosphorylated protein kinase RNA-like endoplasmic reticulum kinase (PERK), phosphorylated eukaryotic initiation factor 2 (eIF2a), and activating transcription factor 4 (ATF4) were significantly increased in rats with IR and attenuated by sevoflurane treatment. The phosphorylation of Akt was further activated by sevoflurane. The cardioprotection of sevoflurane could be blocked by wortmannin, a PI3K/Akt inhibitor. Our results suggest that the cardioprotection of sevoflurane against IR injury might be mediated by suppressing PERK/eIF2a/ATF4/CHOP signaling via activating the Akt pathway, which helps in understanding the novel mechanism of the cardioprotection of sevoflurane. Key words: sevoflurane, cardioprotection, ischemia-reperfusion injury, endoplasmic reticulum stress, Akt. Nous avons vise a etudier si l'effet cardioprotecteur du sevoflurane contre les lesions d'ischemie/reperfusion (IR) est lie a l'inhibition du stress du reticulum endoplasmique. Nous avons obtenu un modele de lesions d'IR myocardique in vivo chez le rat par l'occlusion de l'artere coronaire interventriculaire anterieure. Le sevoflurane a nettement permis d'attenuer le dysfonctionnement cardiaque engendre par les lesions d'IR, ainsi que de faire diminuer le degre d'augmentation de la taille de l'infarctus, des taux de troponine I et de l'activite de la deshydrogenase lactique plasmatiques engendres par les lesions d'IR. Le sevoflurane a permis de faire disparaitre l'apoptose engendree par l'IR dans le myocarde. Le sevoflurane a nettement permis faire diminuer le degre d'augmentation des taux de la proteine 78 regulee par le glucose et de la proteine homologue de la C/EBP (pour << CCAAT/enhancer-binding protein >>) ou CHOP observes apres l'IR myocardique. L'administration de sevoflurane a permis de faire diminuer le degre d'augmentation des taux de proteine PERK (pour << protein kinase RNA-like endoplasmic reticulum kinase >>) phosphorylee, de facteur eIF2a (pour << eukaryotic initiation factor 2 >>) phosphoryle et d'ATF4 (pour << activating transcription factor 4 >>) observees de facon notable chez les rats soumis a l'IR. Le sevoflurane permettait d'activer davantage la phosphorylation de l'Akt. Il etait possible d'inhiber les effets cardioprotecteurs du sevoflurane par la wortmannine, un inhibiteur de la voie de signalisation PI3K/Akt. Nos resultats laissent entendre que les effets cardioprotecteurs du sevoflurane contre les lesions d'IR pourraient etre medies par l'inhibition de l'axe PERK/eIF2a/ATF4/CHOP par l'intermediaire de l'activation de la voie de signalisation de l'Akt, ce qui contribue a la comprehension du nouveau mode d'action des effets cardioprotecteurs du sevoflurane. [Traduit par la Redaction] Mots-cles: sevoflurane, cardioprotection, lesions d'ischemie-reperfusion, stress du reticulum endoplasmique, Akt., Introduction Ischemic heart disease is still one of the leading causes of mortality and morbidity worldwide (Ferdinandy et al. 2007; Xia et al. 2016). Despite the development and improvement of [...]

Cardboard‐like off‐odour in yoghurt can negatively impact consumer acceptability. Herein, a method has been developed to analyse off‐odorants in yoghurt using headspace solid‐phase microextraction coupled with gas chromatography–mass spectrometry. Of 56 volatile organic compounds identified, 8 were active compounds responsible for cardboard‐like off‐odour, including 2, 2‐dimethyl‐propanoic acid and 3‐methyl‐2‐pentanone, which were newly identified in yoghurt. Hexanol and hexanal were found to be indicators of quality deterioration. The off‐odour may be caused by packaging materials and temperature changes during logistic activities. Overall, identifying off‐odorants can help producers to determine which part of the yoghurt‐producing process can be changed to avoid contamination. [ABSTRACT FROM AUTHOR]

Epididymitis can be caused by infectious and noninfectious etiological factors. While microbial infections are responsible for infectious epididymitis, the etiological factors contributing to noninfectious epididymitis remain to be defined. The present study demonstrated that damaged male germ cells (DMGCs) induce epididymitis in mice. Intraperitoneal injection of the alkylating agent busulfan damaged murine male germ cells. Epididymitis was observed in mice 4 weeks after the injection of busulfan and was characterized by massive macrophage infiltration. Epididymitis was coincident with an accumulation of DMGCs in the epididymis. In contrast, busulfan injection into mice lacking male germ cells did not induce epididymitis. DMGCs induced innate immune responses in epididymal epithelial cells (EECs), thereby upregulating the pro-inflammatory cytokines such as tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6), and interleukin-1β (IL-1β), as well as the chemokines such as monocyte chemotactic protein-1 (MCP-1), monocyte chemotactic protein-5 (MCP-5), and chemokine ligand-10 (CXCL10). These results suggest that male germ cell damage may induce noninfectious epididymitis through the induction of innate immune responses in EECs. These findings provide novel insights into the mechanisms underlying noninfectious epididymitis, which might aid in the diagnosis and treatment of the disease. [ABSTRACT FROM AUTHOR]

Objective: To assess the sensitivity and accuracy of a novel transesophageal approach to monitoring the descending aortic oximetry (SeO2)., Methods: Nine dogs were involved in the experimental study. After the induction of anaesthesia, the carrier of the oximetry probe (Nellcor-D20, USA) was inserted into the lower segment of esophagus to monitor SeO2, and the probe was "locked" in position of post-descending aorta after the opening of thoracic cavity. Another probe was pasted on the surface of lingual mucous membrane. The readings and figures of SeO2 and surface of lingual mucosa oximetry (SmO2) were observed continuously and recorded simultaneously. Vital signs were monitored with pulse oxygen saturation (SpO2), invasive blood pressure by femoral artery, HR, EKG, PetCO2, T, FiO2. The SaO2 of blood gas analysis by femoral artery was used as the "gold standard" to calculated the relative and absolute deviations of SeO2 and SmO2. The changes of SeO2 and SaO2 were compared in case of acute hypoxia when values of SmO2 dropped to 90%, 80%, 70%, 60% and the patient was re-ventilated with 100% oxygen., Results: (1) SeO2, SmO2 and SaO2 were 100% when the patients were ventilated with 100% oxygen. During hypoxia, the descent of SeO2 from 100% to 90% was (91.03+/-20.23) s (P<0.001) earlier than that of SmO2. And after re-supply of pure oxygen, the ascent of SeO2 was (25.9+/-6.0) s (P<0.05) earlier than that of SmO2. (2) SaO2 was well related with SeO2 and SmO2 (R2: 0.9884 and 0.9296) respectively. The relative and absolute deviations of SeO2 were 1.6% and 1.3%, while those of SmO2 were 7.6% and 6.1% from arterial blood samples SaO2. (3) There were no significant differences in MAP, HR, ECG, PetCO2 and T., Conclusion: This study showed that SeO2 monitoring is sensitive. It could accurately reflect the arterial oxygen saturation not only in normal condition but also during hypoxia and the re-ventilation with 100% oxygen. SeO2 responds faster and is closer to SaO2, compared with SmO2 measurements. This may be an alternative method in the cases where the monitoring of peripheral SpO2 is difficult.