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This paper focuses on the effects and mechanisms of rare earth and calcium on the flame retardancy of magnesium alloys. Rare earth elements form dense composite oxide films on the surface of the melt, effectively inhibiting the progress of oxidation reactions and significantly increasing the ignition temperature of magnesium alloys. The mechanisms and optimal compositional ranges of different rare earth elements on the flame retardancy of magnesium alloys. Calcium form CaO-rich oxide films in magnesium alloys, which can effectively prevent oxygen diffusion and enhance the flame-retardant resistance of the alloy. When rare earth elements are compounded with calcium, a notable flame-retardant effect is observed. Composite application can maximize the flame-retardant effect of alloy elements while balancing the influence on various properties. Additionally, the authors illustrate through their own research that precise compositional optimization design is required to efficiently exploit the synergistic effects of RE and Ca and mitigate their adverse impacts.

Abstract Background Guillain–Barre syndrome after myocardial infarction occurs infrequently, and its occurrence following percutaneous coronary intervention is extremely rare. Due to the high mortality rate of myocardial infarction and the disability of Guillain–Barre syndrome, early identification of Guillain–Barre syndrome after myocardial infarction and early intervention can decrease the mortality rate, lead to early recovery, and provide a better outcome. Case presentation Herein, we reported a rare case of Guillain–Barre syndrome after myocardial infarction treated with percutaneous coronary intervention. The patient was a 75-year-old woman from China who was admitted to hospital due to sudden loss of consciousness. Electrocardiography showed acute myocardial infarction in the right ventricle and inferior and posterior walls. The patient underwent emergency percutaneous intervention of the posterior collateral artery of the right coronary artery. Soon after, her condition worsened resulting in limb weakness and numbness. Unfortunately, she continued to develop respiratory failure, and treated with intravenous immunoglobulin and ventilator-assisted breathing. A physical examination showed hypotonia of all four limbs, complete quadriplegia, bulbar palsy, dysarthria, and tendon areflexia. Serum immunoglobulin (Ig) G anti-ganglioside antibody analysis was positive with anti-GT1a antibodies (+ +), anti-GM1 antibodies ( +), anti-GM2 antibodies ( +), and anti-GM4 antibodies ( +), and he was diagnosed with Guillain–Barre syndrome after myocardial infarction. She was discharged due to poor response to treatment. The patient died two days after being discharged. Conclusions Myocardial infarction and/or percutaneous coronary intervention may activate immune-mediated response and cause severe complications. Clinician should be alert to Guillain–Barre syndrome after myocardial infarction and/or percutaneous coronary intervention.

Abstract Background Autonomic dysfunctions including bladder dysfunction, gastrointestinal dysfunction and orthostasis are common symptoms of autoimmune glial fibrillary acidic protein astrocytopathy (A-GFAP-A); however, cardiac autonomic dysfunction and abnormal circadian rhythm of blood pressure, which can lead to poor prognosis and even sudden cardiac death, has never been reported in A-GFAP-A patient. Case presentation A 68-year-old male Chinese patient presented to our hospital with headache, fever, progressive disturbance of consciousness, dysuria, and limb weakness. Abnormal heart rate variability and non-dipper circadian rhythm of blood pressure gradually developed during hospitalization, which is rare in A-GFAP-A. He had positive GFAP IgG in cerebrospinal fluid (CSF). Enhanced brian MRI showed uneven enhancement and T2 hyperintense lesions of medulla oblongata; Cervical spine MRI showed T2 hyperintense lesions in medulla oblongata and upper margin of the T2 vertebral body. A contrast-enhanced thoracic spine MRI showed uneven enhancement and T2 hyperintense lesions of T1 to T6 vertebral segments. After treatment with intravenous immunoglobulin and corticosteroids, the patient’s symptoms, including autonomic dysfunction, alleviated dramatically. Finally, his heart rate variability and blood pressure variability became normal. Conclusions Our case broadens the spectrum of expected symptoms in A-GFAP- A syndromes as it presented with heart rate variability and blood pressure variability.

Objective To explore the effect of mechanical ventilation on sublingual microcirculation and right heart function in patients with high altitude pulmonary edema (HAPE). Methods Thirty HAPE patients were randomly divided into HAPE group(conventional treatment) with 14 cases and MV group (mechanical ventilation treatment) with 16 cases, 20 healthy volunteers who did not develop HAPE were randomly selected as the control group. We performed tests including the total of perfused vessel density (TVD), perfused vessel density (PVD), proportion of perfused vessels (PPV) and microcirculation flow index (MFI), left and right diameter of right atrium, anteroposterior diameter of right ventricle, internal diameter of main pulmonary artery, pulmonary artery systolic pressure, blood gas analysis in HAPE group before-after treatment, after healing and in control group. At the same time, the lung rales, lung shadow disappearance time, and clinical cure time were observed in the MV group and HAPE group. Results Compared with the control group, the pH value of the MV group and the HAPE group increased before treatment; blood oxygen saturation (SaO2) decreased; carbon dioxide partial pressure (PaCO2) decreased; blood lactic acid (Lac) increased (P＜0.01). Compared with the HAPE group, the MV group relieved hypoxemia, respiratory alkalosis and reduced blood lactic acid more quickly after 2 h or 6 h treatment(P＜0.05 or P＜0.01). Compared with the control group, the TVD, PVD, PPV and MFI values of the MV group and the HAPE group were significantly lower than those before treatment (P＜0.01). The TVD, PVD, PPV and MFI values of the MV group increased after 24 h treatment, which were better than those of the HAPE group (P＜0.05). Compared with the control group, the left and right atrium diameters of the MV and HAPE groups increased before treatment, the anteroposterior diameter of the right ventricle, the inner diameter of the main pulmonary artery, and the pulmonary artery systolic pressure all significantly increased (P＜0.01). After treatment, the left and right diameters of the right atrium, the anteroposterior diameter of the right ventricle, the internal diameter of the main pulmonary artery, and the systolic pressure of the pulmonary artery all decreased in MV group and HAPE group. After 24-hour treatment, MV group was better than the HAPE group (P＜0.05). Compared with HAPE group, the MV group did shorten the disappearance time of lung rales and shadows, and the clinical cure time (P＜0.01). Conclusions Mechanical ventilation may quickly relieve hypoxemia, significantly improve microcirculation disorders and right heart failure, thereby shorten hospitalization of patients with HAPE.

DOI: 10.3969/j.issn.1672-6731.2017.02.002

Gap junctions (GJ) is an important way to transmit signals among body cells. Studies have confirmed that changes on structure and composition of gap junction proteins are associated with many kinds of diseases. Movement disorders is a common disease of the central nervous system (CNS), which has a certain degree of correlation with GJ, and it has become a key factor in the domestic and foreign research of pathogenesis and treatment mechanism of central nervons system diseases. This paper reviews GJ and its relationship with movement disorders. DOI: 10.3969/j.issn.1672-6731.2016.12.011

Objective To observe the expression of connexin 36 (Cx36) in the striatum and motor cortex of rat model of Parkinson's disease (PD) in order to explore whether gap junction is involved in the pathogenesis of the cortex-basal ganglia circuit disturbances in PD. Methods Hemi-parkinsonian rat model was produced by stereotaxically injecting 6-hydroxydopamine (6-OHDA) to right medial forebrain bundle (MFB). Immunohistochemical staining and Western blotting analysis were used to observe the expression changes of Cx36 in the striatum and motor cortex. Double immunofluorescence labeling was used to analyze the expression of Cx36 in enkephalin (ENK) positive medium spiny neurons and Parvalbumin (PV) positive interneurons in the striatum. Results Immunohistochemical staining showed Cx36 expression was elevated in the right striatum as well as right motor cortex of PD group compared with normal control group (t = 2.474, P = 0.048; t = 2.614, P = 0.040). Double immunofluorescence labeling staining revealed that ENK-positive striatum neurons were elevated (t = 3.987, P = 0.007) and Cx36 expression was increased in ENK-positive striatum neurons (t = 3.271, P = 0.017) in PD group compared with normal control group. While PV-positive interneurons decreased (t = 2.777, P = 0.032) and Cx36 expression was down-regulated in PV-positive interneurons (t = 2.624, P = 0.039) compared with the normal control group. Western blotting indicated that the 6-OHDA lesion induced a significant upregulation of Cx36 to (119.31 ± 8.92)% in comparison with the normal group [(104.05 ± 3.82)%] in right striatum (t = 3.516, P = 0.024). In right motor cortex Cx36 increased to (138.20 ± 17.88)% , induced a significant upregulation of Cx36 in the right motor cortex in comparison with the normal control group [(105.27 ± 2.82)%; t = 4.068, P = 0.015]. Conclusion The Cx36 expression was generally increased in the striatum and motor cortex of PD rat model, with upregulation in ENK-positive striatum neurons but downregulation in PV-positive interneurons, suggesting that gap junction dysfunction may play an important role in the disturbance of cortex-basal ganglia pathway in PD.

Pantothenate kinase ⁃ associated neurodegeneration (PKAN) is a major form of neurodegeneration with brain iron accumulation or NBIA (formerly called Hallervorden ⁃ Spatz syndrome). NBIA is caused by altered neuronal mitochondrial lipid metabolism caused by PANK2 mutations disrupting PANK2 protein levels and catalytic activity and by disrupting maturation and stability of the mitochondrially targeted protein. In this article, we will review advances in inherited and clinical research of PKAN. DOI：10.3969/j.issn.1672⁃6731.2012.03.024

DOI：10.3969/j.issn.1672-6731.2010.03.004