Magnetic Phase Diagram of the MnxFe2-xP1-ySiy System.

The phase diagram of the magnetocaloric MnxFe2-xP1-ySiy quaternary compounds was established by characterising the structure, thermal and magnetic properties in a wide range of compositions (for a Mn fraction of 0.3 ≤ x < 2.0 and a Si fraction of 0.33 ≤ y ≤ 0.60). The highest ferromagnetic transition temperature (Mn0.3Fe1.7P0.6Si0.4, TC = 470 K) is found for low Mn and high Si contents, while the lowest is found for low Fe and Si contents (Mn1.7Fe0.3P0.6Si0.4, TC = 65 K) in the MnxFe2-xP1-ySiy phase diagram. The largest hysteresis (91 K) was observed for a metal ratio close to Fe:Mn = 1:1 (corresponding to x = 0.9, y = 0.33). Both Mn-rich with high Si and Fe-rich samples with low Si concentration were found to show low hysteresis (≤2 K). These compositions with a low hysteresis form promising candidate materials for thermomagnetic applications.

Self-healing polyelectrolyte multilayered coating for anticorrosion on carbon paper.

Ideally, if the corrosion resistance coating on carbon paper (CP) can be endowed with the self-healing property, the service life and the reliability of the carbon paper will be greatly increased as the gas diffusion layer. In this paper, different cycles of s branched poly (ethyleneimine) (bPEI) and poly (acrylic acid) (PAA) were modified on the surface of the carbon paper via layer-by-layer (LbL) self-assembly technology. The prepared polyelectrolyte multilayered coatings can not only protect the carbon fiber from corrosion, but also take advantages of the surrounding water to quickly repair themselves after damaged. The effects of the assembly cycles on morphology, resistance, air permeability and the contact angle of carbon papers were investigated, then the differences of the carbon papers in electrolysis process were explored. The results reveal that all the prepared coatings can protect carbon papers from corrosion, while when the assembly cycles was 10, the coatings are most efficient.

Voltage-dependent blockade by bupivacaine of cardiac sodium channels expressed in Xenopus oocytes.

Bupivacaine ranks as the most potent and efficient drug among class I local anesthetics, but its high potential for toxic reactions severely limits its clinical use. Although bupivacaine-induced toxicity is mainly caused by substantial blockade of voltage-gated sodium channels (VGSCs), how these hydrophobic molecules interact with the receptor sites to which they bind remains unclear. Nav1.5 is the dominant isoform of VGSCs expressed in cardiac myocytes, and its dysfunction may be the cause of bupivacaine-triggered arrhythmia. Here, we investigated the effect of bupivacaine on Nav1.5 within the clinical concentration range. The electrophysiological measurements on Nav1.5 expressed in Xenopus oocytes showed that bupivacaine induced a voltage- and concentration-dependent blockade on the peak of I Na and the half-maximal inhibitory dose was 4.51 µmol/L. Consistent with other local anesthetics, bupivacaine also induced a use-dependent blockade on Nav1.5 currents. The underlying mechanisms of this blockade may contribute to the fact that bupivacaine not only dose-dependently affected the gating kinetics of Nav1.5 but also accelerated the development of its open-state slow inactivation. These results extend our knowledge of the action of bupivacaine on cardiac sodium channels, and therefore contribute to the safer and more efficient clinical use of bupivacaine.

Methanol extract of Phellodendri cortex alleviates lipopolysaccharide-induced acute airway inflammation in mice.

BACKGROUND AND AIM: The effects of methanol extract of Phellodendri cortex on acute airway inflammation induced by intranasal administration of lipopolysaccharide (LPS, 300mug/kg) were investigated in female BALB/c mice. MATERIALS AND METHODS: At 2 h after LPS exposure, mice were treated orally with methanol extract of Phellodendri cortex (100, 200 and 400 mg/kg). At the end of this study, bronchoalveolar lavage fluids (BALF) were collected and number of total cells, macrophages and neutrophils, protein concentration were analyzed. Tumor necrosis factor-alpha (TNF-alpha), macrophage inflammatory protein (MIP-2), IL-10 levels and nitric oxide (NO) production in BALF were also determined. RESULTS: Methanol extract of Phellodendri cortex dose-dependently alleviated LPS-induced acute airway inflammation via decreasing the infiltration of inflammatory cells and the release of inflammatory mediators. CONCLUSION: The relief of airway inflammation provides a possible therapeutic application of Phellodendri cortex for the treatment of infectious pulmonary diseases.

Hydrogen-rich saline reduces lung injury induced by intestinal ischemia/reperfusion in rats.

OBJECTIVE: Hydrogen has been reported to selectively reduce the hydroxyl radical, the most cytotoxic of reactive oxygen species. In this study we investigated the effects of hydrogen-rich saline on the prevention of lung injury induced by intestinal ischemia/reperfusion (I/R) in rats. METHODS: Male Sprague-Dawley rats (n=30, 200-220g) were divided randomly into three experimental groups: sham operated, intestinal I/R plus saline treatment (5ml/kg, i.v.), and intestinal I/R plus hydrogen-rich saline treatment (5ml/kg, i.v.) groups. Intestinal I/R was produced by 90min of intestinal ischemia followed by a 4h of reperfusion. RESULTS: Hydrogen-rich saline treatment decreased the neutrophil infiltration, the lipid membrane peroxidation, NF-kappaB activation and the pro-inflammatory cytokine interleukin IL-1beta and TNF-alpha in the lung tissues compared with those in saline-treated rat. CONCLUSION: Hydrogen-rich saline attenuates lung injury induced by intestinal I/R.

[The clinical application of compound induced hypotension during functional endoscopic sinus surgery].

OBJECTIVE: To assess the clinic efficacy of compound induced hypotension during functional endoscopic sinus surgery. METHOD: Sixty patients with chronic sinusitis and nasal polyps were divided into three groups: Sodium nitroprusside (SNP) group (A), diltiazem+SNP group (B), labetalol+SNP group (C). We started induced hypotension with beginning of functional endoscopic sinus surgery. Mean arterial pressure (MAP), heart rate (HR), cardiac output (CO), cardiac index (CI) and ejection fraction (EF) were recorded during induced hypotension. Sugar and lactic acid in arterial and venous blood were also assayed. Then we calculate rate-pressure product (RPP), arteriovenous difference in blood glucose [D(v-a) BG], blood glucose extraction rate (BGER), arteriovenous difference in lactate [L(v-a)] and lactate produce rate (LPR). RESULT: The dose of SNP applied in group B and C are fewer than group A ( P <0. 05). The cardiovascular functions and body metabolism of the patients in group B and C were stable and the anesthetic effect was satisfactory. Few adverse reaction of the drug was found in present study. CONCLUSION: Induced hypotension with SNP compound of diltiazem or labetalol is an ideal way in clinical use and produce satisfied synergistic effect.

Involvement of GABA and opioid peptide receptors in sevoflurane-induced antinociception in rat spinal cord.

AIM: The spinal cord is pivotal in immobility induced by volatile anesthetics because the anesthetics depress the activity of motor neurons in the spinal cord. The aim of this study was to observe the effects of sevoflurane on pain processing at the spinal level. METHODS: The firing of the gastrocnemius muscle was evoked by electrical stimulation to the ipsilateral hindpaw in rats. The nociceptive C response of electromyography (EMG) was selected to study. The GABAA receptor antagonist bicuculline (0.1 mg/kg) and opioid receptor antagonist naloxone (0.4 mg/kg) were administered intravenously, either in the presence or in the absence of 1.0% sevoflurane. RESULTS: In rats with transected spinal cord, sevoflurane produced a profound reduction in the C response in a dose- and time-dependent manner. In the presence of 1.0% sevoflurane, the C responses were increased after injections of bicuculline and naloxone. CONCLUSION: Sevoflurane is a volatile anesthetic that acts directly on the spinal cord to suppress the nociceptive reflex. The sevoflurane-induced suppression of the C response is antagonized by either bicuculline or naloxone. The results suggest that spinal GABAA receptors and opioid peptide receptors are involved in the sevoflurane-induced suppression of spinal nociception.