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氢气凭借自身独特选择性抗氧化、抗炎等功能以及使用安全性高、制备方便的优势，近年来已被认为是一种新型的抗氧化分子。在糖尿病肾脏病和肾肿瘤并发糖尿病的病理学研究中发现氢气对改善组织损害与延缓病变加剧有积极作用，有望成为一种新型的气体分子靶点。本文就近年来氢气改善上述疾病的基础性研究与临床试验中的病理学研究进展作一综述，为进一步明确氢分子改善肾脏损伤与疾病诊断和组织学分析评价提供参考。.

One 51 years old man was admitted to the rheumatology department with a history of prominent eyes, headache and blurred vision for half year. The main manifestations included retrobulbar inflammatory pseudotumor and retroperitoneal fibrosis. He was initially diagnosed as granulomatosis with polyangiitis. Prednisone and cyclophosphamide were administrated and effective. New mass of dura mater and osteosclerosis presented during follow up. Finally Erdheim Chester disease(ECD) was diagnosed by biopsy and pathological examination. Vemurafenib, a v-raf murine sarcoma viral oncogenes homolog B1 (BRAF) inhibitor, 480 mg was given twice a day. The patient's condition is stable and still in follow-up. Although ECD is a rare histiocytosis, clinicians should pay attention to its manifestations and differential diagnoses.患者男性，51岁。因双眼突出、头痛、视物模糊半年就诊。主要临床特征为球后炎性假瘤及腹膜后纤维化，初诊为肉芽肿性多血管炎（GPA），先后予地塞米松10 mg/d静脉输液5 d，口服泼尼松1 mg·kg

Acute lung injury (ALI) is a clinical problem with poor prognosis and high mortality. The purpose of this study was to explore the effects of helix B position peptide (HBSP) on ALI and its mechanism.C57/BL6 male mice were used to construct ALI models by LPS tracheal injection and detect the effect of HBSP on mouse ALI by subcutaneously injecting HBSP. In addition, normal human lung epithelial cell line (BEAS-2B) were cultured and stimulated with HBSP. Then, the effects of HBSP on oxidative stress and endoplasmic reticulum stress (ERS) in BEAS-2B cells were examined. Finally, the effect of HBSP on the Nrf2/HO-1 signaling pathway was examined, and the mechanism of action of HBSP was verified using the Nrf2/HO-1 signaling pathway inhibitor ML385.In vitro, HBSP increased the expression of SOD1/2 and decreased the expression of ERS-related molecules such as CHOP, GRP-78, and caspase-12, indicating that HBSP effectively reduces the level of oxidative stress and ERS in BEAS-2B cells. In addition, HBSP also increased the activity of the Nrf2/HO-1 signaling pathway and ML385 reduced the protective effect of HBSP on BEAS-2B cells. In vivo, HBSP significantly reduced LPS-induced mouse ALI. W/D and inflammatory factors in the BALF of the mouse lung were significantly reduced and the level of oxidative stress was also reduced.HBSP plays an important role in relieving ALI by activating Nrf2/HO-1 signaling pathway, which reduces the level of inflammation in lung tissue and oxidative stress and ERS in lung epithelial cells.

The aim of this study was to explore the potential effect of miRNA-1297 on myocardial fibrosis (MF) and its underlying mechanism.MF model was established by cardiac perfusion of Angiotensin II (Ang-II) in mice. The primary myocardial fibroblasts were extracted from MF mice (Ang-II infusion group) and controls (sham group), respectively. The relative levels of miRNA-1297 and ULK1 in the in vivo and in vitro MF models were determined by quantitative Real Time-Polymerase Chain Reaction (qRT-PCR). Meanwhile, the protein expressions of fibrosis-related genes in MF mice and primary myocardial fibroblasts were determined by Western Blot. Subsequently, the Dual-Luciferase Reporter Gene Assay was applied to verify the downstream gene of miRNA-1297. In addition, a series of rescue experiments were conducted to elucidate the role of miRNA-1297/ULK1 in regulating MF.Masson staining showed plenty of micro-vessels around myocardial tissues and significantly increased contents of intercellular collagen in Ang-II infusion group when compared with those in the sham group. Western blot results revealed that the protein expressions of Col1a1 and α-SMA were significantly upregulated in myocardial tissues of MF mice. QRT-PCR data illustrated that miRNA-1297 was remarkably downregulated in MF model. ULK1 was verified as the target gene of miRNA-1297, which was upregulated in the MF model. The overexpression of miRNA-1297 or the knockdown of ULK1 could downregulate the protein levels of Col1a1 and α-SMA in primary myocardial fibroblasts extracted from MF mice. Notably, ULK1 overexpression could reverse the regulatory effect of miRNA-1297 on MF.MiRNA-1297 suppresses myocardial fibrosis via down-regulating ULK1.

Hepatocellular carcinoma (HCC) is one of the most commonly diagnosed cancers globally. LncRNA HLA complex group 11 (HCG11) has been reported to play an oncogenic role in multiple cancers. Nevertheless, the role and regulatory mechanism of HCG11 in HCC are not fully addressed.The abundance of HCG11 and miR-26a-5p was measured by quantitative Real Time-Polymerase Chain Reaction (qRT-PCR) in HCC tissues and cells. Cell proliferation, apoptosis, metastasis, and autophagy were detected by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT), flow cytometry, transwell migration, invasion assays, and Western blot assay, respectively. The binding sites between miR-26a-5p and HCG11 or autophagy-related 12 (ATG12) were predicted by starBase bioinformatic software, and the combination was confirmed by Dual-Luciferase reporter assay. The abundance of ATG12 was examined by Western blot assay. Murine xenograft model was established to validate the function of HCG11 in vivo.The enrichment of HCG11 was enhanced in HCC tissues and cells and was negatively related to the prognosis of HCC patients. The abundance of miR-26a-5p was inversely correlated with the level of HCG11 in HCC tissues. HCG11 interference suppressed the proliferation, metastasis, and autophagy while promoted the apoptosis of HCC cells. MiR-26a-5p bound to lncRNA HCG11 and ATG12. The depletion of miR-26a-5p or the accumulation of ATG12 could alleviate the suppressive effects induced by HCG11 intervention on the proliferation, metastasis, autophagy, and the promoting impact on the apoptosis of HCC cells. HCG11 promoted the growth of murine xenograft tumor and autophagy through miR-26a-5p/ATG12 axis in vivo.LncRNA HCG11 accelerated the proliferation, metastasis, and autophagy while impeded the apoptosis of HCC cells via HCG11/miR-26a-5p/ATG12 axis. HCG11 might be a potential therapeutic target for the treatment of HCC.

This study was to investigate expression levels and functional activities of histone deacetylases (HDACs) with potential therapeutic targets selected in animal model of allergic asthma. Mice were sensitized and then challenged with saline (control) or ovalbumin (OVA) for 8 weeks. Airway resistance was determined by increasing concentrations of acetyl-β-methacholine chloride (0 - 50 mg/ml). The number of cells and cytokine production in bronchoalveolar lavage fluid (BALF) were determined by ELISA. Pathological changes of lung specimens were examined by histochemical staining methods under the light microscope. Expression and quantification of HDACs in lungs were measured using immunohistochemistry and Western blotting analysis. HDAC activity was identified using colorimetric and fluorometric methods. The OVA-treated mice had a significant enhancement in airway resistance with a large number of cells and increased interleukin (IL)-4 and -5 levels in BALF. Morphologically, an infiltration of inflammatory cells into epithelial layer with mucus accumulation and subepithelial fibrosis were seen in the OVA-exposed lungs. The expression levels for HDAC1, HDAC5, HDAC6, and HDAC8 were significantly elevated with weak induction of HDAC 2-4, which was identical with their catalytic activities detected in the lungs. In contrast, HDAC1 and HDAC5 activities were higher than others in the lungs. Individual HDACs are differently regulated in expression levels and functional activities in animal model of allergic asthma. Selective targeting of HDAC1/5 offers an opportunity to improve therapeutic effects of the disease.

Human health and diseases are determined by many complex factors. Health threats from the human-animal-ecosystems interface (HAEI) and zoonotic diseases (zoonoses) impose an increasing risk continuously to public health, from those emerging pathogens transmitted through contact with animals, food, water and contaminated environments. Immense challenges forced on the ecological perspectives on food and the eco-environments, including aquaculture, agriculture and the entire food systems. Impacts of food and eco-environments on human health will be examined amongst the importance of human interventions for intended purposes in lowering the adverse effects on the biodiversity. The complexity of relevant conditions defined as factors contributing to the ecological determinants of health will be illuminated from different perspectives based on concepts, citations, examples and models, in conjunction with harmful consequential effects of human-induced disturbances to our environments and food systems, together with the burdens from ecosystem disruption, environmental hazards and loss of ecosystem functions. The eco-health literacy should be further promoting under the “One Health” vision, with “One World” concept under Ecological Public Health Model for sustaining our environments and the planet earth for all beings, which is coincidentally echoing Confucian’s theory for the environmental ethics of ecological harmony.

Two humic-like substances, the oxidative polymer of protocatechuic acid (OP-PCA) and humic acid inhibit the in vitro replication of influenza virus A/WSN/33 (H1N1) in Madin-Darby canine kidney (MDCK) cells at concentrations of no cytotoxicity. The 50% inhibitory concentration (IC50) for OP-PCA was 6.59 +/- 1.02 microg/ml when the compound was added at the stage of viral adsorption. When OP-PCA was added after virus adsorption, the IC50 was 53.27 +/- 8.12 microg/ml. The IC50 for humic acid was 48.61 +/- 7.32 microg/ml and 55.27 +/- 5.46 microg/ml respectively when the compound was added at the stage of viral adsorption or post-adsorption. In spite of structural resemblance of these two compounds, they exhibit different actions of anti-flu. The OP-PCA inhibits virus-induced hemagglutination and low pH-induced cell-cell fusion. Humic acid inhibits the endonuclease activity of viral RNA polymerase. The monomer of PCA shows no inhibition on influenza virus replication.

To study the mechanism of the effect of gonadotropin-induced oocyte maturation.Mouse oocytes were cultured in HX-medium, and the effects of amphotericin B and ketoconazole on resumption of meiosis of mouse oocyte were examined.1. FSH(10-200 IU/L) induced a dose-dependent manner of oocytes maturation in CEO. A maximum increase in GVBD was observed with 25-50 IU/L FSH. 2. Amphotericin tericim B (0.025-2.5 micrograms/L) caused significant increases in GVBD in CEO, which mimicked the function of FSH. 3. Ketoconazole (10(-7)-10(-3) mol/L) inhibited the effect of FSH on resumption of meiosis, but no effect on oocyte spontaneous maturation.Amphotericin B and ketoconazole are able to affect mouse oocyte maturation, and indicates that they have a regulation on FSH-induced synthesis of meiosis-activating sterol.

Based on the consistency of the in vivo and in vitro interactions of drugs with DNA, a fluorimetric method has been developed as a new in vitro method for preliminary screening of antitumour agents. This method was tested using Schiff bases synthesized from salicylaldehyde with 1-alanine, 1-asparagine and 1-histidine, and complexes of these Schiff bases with Cu(II), Zn(II), Ni(II) and Sn(IV) as potential antitumour agents. The study of the interaction of the complexes with DNA by a fluorescence probe ethidium bromide (EthBr)-DNA system indicated the parallelism between the binding constants and antineoplastic ratios. The relationship between structure and antitumour activity was investigated.

The effect of combined cyclophosphamide (CY) and heat treatments on a murine tumor was studied at various temperatures. FSa-II tumors, the early generation isotransplants of a spontaneous fibrosarcoma in a C3Hf/Sed mouse, were used. A single cell suspension was transplanted into the animal foot. Hyperthermia was given by immersing animal feet into a water bath maintained at a desired temperature +/- 0.1 degrees C. An average diameter of the tumor at the time of treatment was 4 mm. The tumor growth time, the time required for one-half of the treated tumors to reach 1000 mm3, was the end point. Hyperthermia enhanced the effect of CY at test temperatures ranging from 40.5 degrees - 44.5 degrees C. The enhancement was independent of the temperature when CY was administered 30 min before the beginning of hyperthermia. However, the enhancement was most substantial at temperatures of 40.5 degrees -42.5 degrees C when CY was administered immediately before hyperthermia. The most effective timing of the CY administration was immediately before hyperthermia. The glucose administered 60 min before hyperthermia enhanced the effect of combined CY and hyperthermia when CY was given 30 min before heating. This enhancement was lost when CY was given immediately before hyperthermia. The CY dose response curves at elevated temperatures were downward concave, which may indicate the presence of a CY- and heat-resistant cell population in the tumor. Implications of these observations in clinical hyperthermia were discussed.

Summary. – The herpes simplex virus type 1(HSV-1) tegument protein VP22 encoded by the UL49 gene is essential for HSV-1 infection. However, its precise functions in the virus life cycle are unknown. A relatively important tool for disclosing these functions is an antiserum specifically detecting VP22 in the infected cell. To this end, a recombinant truncated VP22 protein consisting of C-terminal 45 aa fused to EYFP (enhanced yellow fluorescent protein) and His-tag was expressed in Escherichia coli , purified by the Ni 2+ -NTA affinity chromatography, and used for the preparation of antiserum in rabbits. Western blot and immunofluorescence assay showed that this antiserum specifically detected purified truncated VP22 as well as full-length VP22 in the HSV-1 infected cells. These results indicate that the prepared antiserum could serve as avaluable tool for further studies of VP22 functions. Keywords: herpes simplex virus type 1; truncated VP22; E. coli; recombinant protein; EYFP; antiserum