Synthesis and evaluation of Mn-Sn modified Ru-Ir electrode for electrocatalytic treatment of high chloride acrylonitrile wastewater.

Acrylonitrile wastewater was an organic wastewater with strong toxicity and poor biodegradability. Therefore, electro-catalytic technology became a promising acrylonitrile wastewater treatment technology because of no secondary pollution, wide application range and low water quality requirements. The optimal Mn-Sn modified Ru-Ir electrode material was synthesized by thermal method and applied in electro-catalytic treatment of acrylonitrile wastewater. The electrode materials were characterized by SEM, TEM, XRD, XPS and electrochemical characterization. SEM, TEM, XRD and XPS indicated that Mn and Sn were capable of incorporating and replacing the part of Ru or Ir and could alter the microstructure of Ru-Ir and the types of Mn and Sn oxides, raising the oxygen evolution potential (OEP) and voltampere charge. When the molar ratio of Mn-Sn was 1:1, OEP, voltampere charge and exchange current density could reach 1.303 V, 1.51 C/cm2 and 6.29×10-4 A/cm2, respectively. The co-doping of Mn-Sn had significant influence on the electrocatalytic performance of Ru-Ir electrode materials. The optimum synthesis conditions of Mn-Sn modified Ru-Ir electrode were as follows: the molar ratio of Mn-Sn was 1:1, calcination time was 4.0 hours, calcination temperature was 450℃, and solvent was water. Under certain conditions, the removal rate of acrylonitrile with Mn-Sn modified Ru-Ir electrode was 100%. Mn-Sn modified Ru-Ir electrode had high oxygen evolution potential and good removal effect of acrylonitrile, which was higher than that of ruthenium iridium electrode and RuO2 electrode.

Preparation and evaluation of Pd-Sn modified Ru-Ir electrode for denitrification of high chlorine ammonia-nitrogen wastewater.

In this paper, Pd-Sn modified Ru-Ir electrode was prepared by thermal oxidation method, and the effects of doping amount of Pd-Sn and synthesis conditions on Pd-Sn modified Ru-Ir electrode performance were studied. Linear sweep voltammetry(LSV), cyclic voltammetry(CV), and the Tafel curve were used to study the electrochemical performance of the Pd-Sn modified Ru-Ir electrode materials. The effects of the doping amount of Pd-Sn on the microstructure and valence states of Pd-Sn modified Ru-Ir electrode materials were investigated by SEM, TEM, XRD, and XPS. When the mass of Pd-Sn accounted for 1.5% of the total mass of the elements, the molar ratio of Ru-Ir was 2:1, and the molar ratio of Pd-Sn was 3:1; the LSV, CV, and the Tafel curves indicated that Pd-Sn modified Ru-Ir electrode had the lowest chlorine evolution potential (1.0640 V vs. SCE), the best CV curve coincidence, and the smallest corrosion current density (6.5 × 10-4 A/cm2), showing the best chlorine evolution performance, the best durability, and corrosion resistance; the characterization of SEM, TEM, XRD, and XPS showed that Pd-Sn was successfully doped into Ru-Ir electrode materials; the crystallinity of Pd-Sn modified Ru-Ir electrode was the highest, and the binding energy was the lowest, but the crystal form of Ru-Ir solid solution did not have changed. The optimal synthesis conditions of Pd-Sn modified Ru-Ir electrode material were as follows: Pd-Sn molar ratio was 3:1, calcination temperature was 500 ℃, calcination time was 4 h, and water was used as solvent. Pd-Sn modified Ru-Ir electrode can efficiently treat high chlorine ammonia-nitrogen wastewater, when the reaction volume was 200 mL, the initial concentration of NH3-N was 100 mg/L, the concentration of chloride ion was 5000 mg/L, the current was 0.75 A, and the reaction time was 40 min; the removal rate of ammonia nitrogen can reach 100%.Responsible editor: Weiming Zhang.

Anesthetic management of lung transplantation in a patient with end-stage COVID-19 pneumonia: A case report.

RATIONALE: The COVID-19 pandemic is spreading around the world and the leading cause of death is rapidly progressive respiratory failure because of lung damage and consolidation. Lung transplantation is the last line of treatment for chronic end-stage lung diseases. There were several cases of lung transplantation reported in patients with COVID-19 pneumonia. However, anesthetic management of lung transplantation in this subpopulation is rare. We report the anesthetic and perioperative management of lung transplantation in a patient with COVID-19 pneumonia. PATIENT CONCERNS: A 70-year-old man with a 7-day history of fever was diagnosed with COVID-19 pneumonia. His throat swab was positive for COVID-19, but negative for other common viruses. Chest radiography showed multiple inflammatory foci in both lungs. By day 5, he presented respiratory distress. Computed tomography (CT) scan showed progressive deterioration of both lungs. Starting on day 7, SARS-CoV-2 RNA in bronchoalveolar lavage samples were continuously negative. However, his lung condition deteriorated. By day 17, a veno-venous extracorporeal membrane oxygenation (ECMO) was initiated. After 10 days of ECMO support, the patient's lung condition did not improve. CT scan revealed bilateral parenchymal consolidation with pulmonary fibrosis and hydrothorax. DIAGNOSIS: Irreversible lung function loss induced by COVID-19 pneumonia. INTERVENTIONS: Bilateral transplantation was performed because the patient's lung condition did not improve and CT scan revealed parenchymal consolidation with pulmonary fibrosis after 10 days of ECMO support. Thirty-six hours after the surgery, ECMO was discontinued. A percutaneous transluminal coronary angioplasty and a stent implantation were performed because of acute coronary syndrome and myocardial ischemia 4 days postoperatively. OUTCOMES: The patient remained hospitalized because of requirements for intermittent assisted ventilation via tracheostomy. LESSONS: This case further supports the consideration that lung transplantation can potentially be the successful therapy for these patients who have developed irreversible lung function lose due to COVID-19 pneumonia. However, most critical patients with COVID-19 are older individuals with various comorbidities, which present new anesthetic challenges.

Silencing of spinal Trpv1 attenuates neuropathic pain in rats by inhibiting CAMKII expression and ERK2 phosphorylation.

Accumulating evidence suggests a potential role of transient receptor potential vanilloid 1 (TRPV1) channels in inflammatory and cancer-related pain. However, the role of TRPV1 in the maintenance of neuropathic pain remains elusive. The current study investigated the effects of transient Trpv1 gene silencing using a small interference RNA (siRNA) on neuropathic pain induced by chronic constriction injury (CCI) of the sciatic nerve in rats. Seven days after CCI, the TRPV1 siRNA was intrathecally administered (5 µg/15 µl, once daily for 2 days). TRPV1 and Ca2+/calmodulin-dependent protein kinase II (CAMKII) expression and extracellular signal-regulated kinase (ERK) phosphorylation in the spinal cord were detected using western blotting. The thresholds to mechanical and thermal stimuli were determined before and after intrathecal TRPV1 siRNA administration. TRPV1 and CAMKII expression and ERK2 phosphorylation in the spinal cord were upregulated after CCI. Intrathecal administration of the TRPV1 siRNA not only attenuated behavioural hyperalgesia but also reduced the expression of TRPV1 and CAMKII, as well as ERK2 phosphorylation. Based on these results, silencing of the TRPV1 gene in the spinal cord attenuates the maintenance of neuropathic pain by inhibiting CAMKII/ERK2 activation and suggests that TRPV1 represents a potential target in pain therapy.

Additive analgesic effect of dexmedetomidine and dezocine administered intrathecally in a mouse pain model.

BACKGROUND: It is known that dexmedetomidine can reduce opioid requirements and that there is a synergistic effect when dexmedetomidine and morphine (a full mu opioid receptor agonist) are administered together. However, it was unclear whether a synergistic or additive effect would be observed when dexmedetomidine was co-administered with a partial mu opioid receptor agonist. The present study was designed to elucidate such effects by intrathecally co-administering dexmedetomidine and dezocine, a partial mu receptor agonist, in a mouse pain model. METHODS: C57 mice (N = 165) were randomly divided into 19 groups. The tail flick test was adopted to measure the antinociceptive effects of the tested agents. The mice were divided into saline and drug groups to investigate the dose-dependent analgesic effects. Each drug was administered at fixed doses alone and in combination with one of three doses of a second drug. RESULTS: Dezocine (0.3125 - 1.25 µg) and dexmedetomidine (0.04 - 1 µg) both enhanced the tail withdrawal latency in dose-dependent fashions. Dexmedetomidine (0.04 - 1 µg) enhanced the analgesic effect of dezocine. Dezocine (0.3125 - 1.25 µg) enhanced the analgesic effect of dexmedetomidine. Compared with the individual drug effects, the combined effects of dezocine (0.625 µg) and dexmedetomidine (0.04 µg) were more potent 15 - 60 min after injection, but they remained similar to the sum of the effects of the two individual drugs. CONCLUSIONS: Dexmedetomidine and dezocine produce an additive analgesic effect on acute nociception when administered simultaneously.

N-methyl D-aspartate receptor subtype 2B antagonist, Ro 25-6981, attenuates neuropathic pain by inhibiting postsynaptic density 95 expression.

Postsynaptic density-95 (PSD-95) is a synaptic scaffolding protein that plays a crucial role in the development of neuropathic pain. However, the underlying mechanism remains unclear. To address the role of PSD-95 in N-methyl-D-aspartate receptor subtype 2B (NR2B) -mediated chronic pain, we investigated the relationship between PSD-95 activation and NR2B function in the spinal cord, by using a rat model of sciatic nerve chronic constriction injury (CCI). We demonstrate that the expression levels of total PSD-95 and cAMP response element binding protein (CREB), as well as phosphorylated NR2B, PSD-95, and CREB, in the spinal dorsal horn, and the interaction of NR2B with PSD-95 were increased in the CCI animals. Intrathecal injection of the selective NR2B antagonist Ro 25-6981 increased paw withdrawal latency, in a thermal pain assessment test. Moreover, repeated treatment with Ro 25-6981 markedly attenuated the thermal hypersensitivity, and inhibited the CCI-induced upregulation of PSD-95 in the spinal dorsal horn. Furthermore, intrathecal injection of the PSD-95 inhibitor strikingly reversed the thermal and mechanical hyperalgesia. Our results suggest that blocking of NR2B signaling in the spinal cord could be used as a therapeutic candidate for treating neuropathic pain.

Dezocine Antagonizes Morphine Analgesia upon Simultaneous Administration in Rodent Models of Acute Nociception.

BACKGROUND: Dezocine is a powerful analgesic that can be less addictive than morphine, yet how the two drugs interact in vivo is poorly understood. Here we administered dezocine alone or in combination with morphine to different acute nociception paradigms to explore the interactions of the 2 drugs upon co-administration. OBJECTIVE: To evaluate how dezocine interacts with morphine in different acute nociception paradigms. STUDY DESIGN: Laboratory animal study. SETTING: Zhejiang University School of Medicine, Hangzhou, China. METHODS: Healthy mice were treated with saline, dezocine (0.625 - 2.5 µg), or a combination of dezocine with morphine (2.5 µg). Tail withdrawal latency (TWL) was analyzed prior to and 30 minutes after drug administration. Rats were treated with saline, morphine (3 mg/kg), dezocine (3 mg/kg), or a combination of both drugs. The animals were then left uninjured, subjected to plantar incision, or underwent formaldehyde-induced acute inflammation. Nociception was then analyzed in terms of mechanical threshold (MT) to von Frey stimulation and paw withdrawal latency (PWL) to thermal stimulation. Formaldehyde-induced pain score was calculated based on the duration of biting and elevating of the animal's legs. Phosphorylation of extracellular signal-regulated kinase (pERK) was also measured after plantar incision as a molecular index of nociception. RESULTS: Dezocine enhanced TWL but inhibited morphine analgesia in a dose-dependent fashion in mice. Usage of morphine or dezocine alone in uninjured rats increased MT, but co-administering both drugs did not further increase MT. Usage of one drug alone, and both drugs together increased MT and PWL relative to saline at 30 minutes after incision. Usage of one drug alone, but not both drugs together, increased MT and PWL at 120 minutes after incision. Dezocine reduced formaldehyde-induced nociception but co-administering both drugs did not further reduce pain behavior. LIMITATIONS: The results were obtained from animal study; clinical investigations will be needed to clarify their interaction. CONCLUSION: Dezocine antagonizes morphine analgesia on acute nociception upon simultaneous administration.Key words: Dezocine, morphine, acute nociception, analgesia.

Spinal synaptic scaffolding protein Homer 1b/c regulates CREB phosphorylation and c-fos activation induced by inflammatory pain in rats.

Previous studies have shown that spinal Homer 1b/c plays an important role in the maintenance of chronic inflammatory pain induced by complete Freund's adjuvant (CFA). This study investigated the possible mechanism underlying Homer 1b/c mediating CFA-induced inflammatory pain. Chronic inflammation was induced by CFA injection into the left hind ankle of the rat. Homer 1b/c antisense or missense oligonucleotides were administered intrathecally (10µg/10µl) from 5 to 8 days following the onset of inflammation. Immunohistochemistry was conducted to detect the expression of phosphorylated cAMP response element binding protein (pCREB) and Fos protein in the spinal dorsal horn. Intrathecal administration of Homer 1b/c antisense oligonucleotides not only markedly reduced the expression of Homer 1b/c protein, but also attenuated CFA-induced inflammation, spinal CREB phosphorylation, and Fos expression. These results demonstrate for the first time that Homer 1b/c regulates CREB phosphorylation and c-fos activation in the spinal dorsal horn during the maintenance of chronic inflammatory pain, suggesting that Homer 1b/c may be involved in the development of CFA-induced inflammation.

Cloning and characterization of a balsam pear class I chitinase gene (Mcchit1) and its ectopic expression enhances fungal resistance in transgenic plants.

A balsam pear (Momordica charantia L.) chitinase (Mcchit1) was purified and sequenced at the N-terminal. The genomic and cDNA coding sequences of Mcchit1 were cloned by rapid amplification of 3' cDNA ends (3'-RACE) and the Y-shaped adaptor dependent extension (YADE) method. Sequence analysis showed that the Mcchit1 protein is a class I chitinase containing a chitin-binding domain and a catalytic domain, but no C-terminal extension. Northern blot indicated that the Mcchit1 transcription is wound-inducible. Overexpression of Mcchit1 dramatically increased intercellular and intracellular endochitinase activities, suggesting that the Mcchit1 gene encodes a secretory endochitinase. It was also found that overexpression of Mcchit1 significantly enhanced resistance to the plant pathogenic fungus Phytophthora nicotianae in transgenic N. benthamiana plants and against Verticillium wilt in transgenic cottons, indicating that the Mcchit1 gene can be a useful gene in plant engineering against fungal diseases.