[Clinical features, diagnosis and treatment of 5 cases of primary pneumonic plague in Tibet in 2010].

OBJECTIVE: To explore the clinical manifestations, the feature of chest X-ray, the clinical outcome, and the clinical treatments of severe pneumonic plague. METHODS: We observed the clinical course of primary pneumonic plague in 5 patients, who infected Yersinia pestis in Tibet during September 2010, including manifestations of chest X-ray, the antibiotic therapy, respiratory support and the prognosis. RESULTS: All of the 5 patients presented with high fever, bloody sputum and difficulty breathing. The chest X-ray showed signs consistent with necrotizing inflammation with multiple lobar involvement. Mass-like lesions might coalesce, and the "white lung" sign might appear. Three out of the 5 patients presented with hypoxemia. The results of reverse indirect hemagglutination assay (RIHA) in these patients were positive on the second day of the illness onset. All of these patients recovered after antibiotic therapy and other treatments. However, the absorption of lung lesions was very slow. CONCLUSIONS: Patients infected with primary pneumonic plague presented with rapid onset high fever and hemoptysis, and the lung injury was very severe. The positive result of RIHA was useful for early diagnosis of plague. Streptomycin should be the first choice for Yersinia pestis infection, but its optimal dose needed further study. Fluoroquinolones can be used as combination with Streptomycin. Nutritional support and symptomatic treatment, as well as non-invasive or invasive mechanical ventilation when needed, were important for the management of the disease.

Whole-Genome Sequencing Identifies the Egl Nine Homologue 3 (egln3/phd3) and Protein Phosphatase 1 Regulatory Inhibitor Subunit 2 (PPP1R2P1) Associated with High-Altitude Polycythemia in Tibetans at High Altitude.

BACKGROUND: The hypoxic conditions at high altitudes are great threats to survival, causing pressure for adaptation. More and more high-altitude denizens are not adapted with the condition known as high-altitude polycythemia (HAPC) that featured excessive erythrocytosis. As a high-altitude sickness, the etiology of HAPC is still unclear. METHODS: In this study, we reported the whole-genome sequencing-based study of 10 native Tibetans with HAPC and 10 control subjects followed by genotyping of selected 21 variants from discovered single nucleotide variants (SNVs) in an independent cohort (232 cases and 266 controls). RESULTS: We discovered the egl nine homologue 3 (egln3/phd3) (14q13.1, rs1346902, P = 1.91 × 10-5) and PPP1R2P1 (Protein Phosphatase 1 Regulatory Inhibitor Subunit 2) gene (6p21.32, rs521539, P = 0.012). Our results indicated an unbiased framework to identify etiological mechanisms of HAPC and showed that egln3/phd3 and PPP1R2P1 may be associated with the susceptibility to HAPC. Egln3/phd3b is associated with hypoxia-inducible factor subunit α (HIFα). Protein Phosphatase 1 Regulatory Inhibitor is associated with reactive oxygen species (ROS) and oxidative stress. CONCLUSIONS: Our genome sequencing conducted in Tibetan HAPC patients identified egln3/phd3 and PPP1R2P1 associated with HAPC.

Transcriptome Reveals 1400-Fold Upregulation of APOA4-APOC3 and 1100-Fold Downregulation of GIF in the Patients with Polycythemia-Induced Gastric Injury.

High-altitude polycythemia (HAPC) inducing gastric mucosal lesion (GML) is still out of control and molecular mechanisms remain widely unknown. To address the issues, endoscopy and histopathological analyses were performed. Meanwhile, microarray-based transcriptome profiling was conducted in the gastric mucosa from 3 pairs of healthy subjects and HAPC-induced GML patients. HAPC caused morphological changes and pathological damages of the gastric mucosa of GML patients. A total of 10304 differentially expressed genes (DEGs) were identified, including 4941 up-regulated and 5363 down-regulated DEGs in gastric mucosa of GML patients compared with healthy controls (fold change ≥2, P<0.01 and FDR <0.01). Particularly, apolipoprotein genes APOA4 and APOC3 were 1473-fold and 1468-fold up-regulated in GML patients compared with the controls. In contrast, gastric intrinsic factor (GIF) was 1102-fold down-regulated in GML patients compared with the controls. APOA4 (chr11:116691770-116691711), APOC3 (chr11:116703530-116703589) and GIF (chr11:59603362-59603303) genes are all located on chromosome 11. APOA4 and APOC3 act as an inhibitor of gastric acid secretion while gastric acid promotes ulceration. GIF deficiency activates a program of acute anemia, which may antagonize polycythemia while polycythemia raises the risk of GML. Therefore, the present findings reveal that HAPC-induced GML inspires the protection responses by up-regulating APOA4 and APOC3, and down-regulating GIF. These results may offer the basic information for the treatment of HAPC-induced gastric lesion in the future.

Use of additives in the electrodeposition of nanostructured Eu3+/ZnO films for photoluminescent devices.

Rare-earth ion-doped ZnO has been the focus of numerous investigations because of its unique optical properties and promising applications in optoelectronic devices. Here we presented a facile electrochemical deposition route for the controllable preparation of Eu3+/ZnO nanostructures on a large scale. The prepared Eu3+/ZnO deposits were characterized by scanning electron microscopy, energy dispersive spectroscopy, X-ray diffraction, selected area electron diffraction, and X-ray photoelectron spectroscopy. Herein, the growth mechanisms of Eu3+/ZnO nanosheets and nanorods were discussed. The formation process of Eu3+/ZnO foam-like nanostructures is illuminated in this paper. The room temperature photoluminescence properties of the Eu3+/ZnO foam-like nanostructures were investigated. The sharp 4f-4f transition emissions of Eu3+ can be directly observed at 593, 617, and 698 nm. An energy transfer between ZnO and Eu3+ is shown to occur under UV excitation.