A new secondary metabolite from the marine-derived fungus Phomopsis lithocarpus FS508.

Based on the One Strain-Many Compounds (OSMAC) strategy, the secondary metabolites of Phomopsis lithocarpus FS508 were investigated. As a result, a new secondary metabolite, 4-methoxy-3-[4-(acetyloxy)-3-methyl-2-butenyl]benzoic acid (1) as well as eleven known compounds were isolated from the fermentation product of the strain FS508. Their structures were determined by NMR, IR, UV, and MS spectroscopic data analyses. All the isolated compounds were evaluated for cytotoxic and anti-inflammatory activities. Among them, compounds 3 and 9 displayed potent cytotoxicity against HepG-2 cell line, and compounds 2, 3 and 12 showed significant anti-inflammatory activities.

Eutypellacytosporins A-D, Meroterpenoids from the Arctic Fungus Eutypella sp. D-1.

The Arctic fungus Eutypella sp. D-1, previously found to produce a variety of cytotoxic cyclopropyl-fused and cyclobutyl-fused pimarane diterpenoids when grown in the defined medium, was induced to produce unusual metabolites by growing on solid rice medium. A chemical investigation on the rice medium extract led to the isolation of four new meroterpenoids, eutypellacytosporins A-D (1-4), along with the known biogenetically related compound cytosporin D (5). The structures of the new compounds were elucidated by their detailed spectroscopic analysis and modified Mosher's method. Compounds 1-4 may be formed by the 12,32-ester linkage of two moieties, cytosporin D (5) and decipienolide A or B. All isolated compounds, except 5, showed weak cytotoxicity against DU145, SW1990, Huh7, and PANC-1 cell lines with IC50 values ranging from 4.9 to 17.1 µM.

Bioactive metabolites from the Arctic fungus Nectria sp. B-13.

Two new cyclohexanone derivatives, nectriatones A-B (1-2), and one new natural product, nectriatone C (3), together with three known phenolic sesquiterpene derivatives (4-6), were isolated from the culture of Nectria sp. B-13 obtained from high-latitude soil of the Arctic. The structures of all compounds were unambiguously elucidated by extensive spectroscopic analysis, as well as by comparison with the literature. These compounds were evaluated in cytotoxic and antibacterial activities. Compounds 1-6 showed cytotoxicities against SW1990, HCT-116, MCF-7, and K562 cells, with IC50 values in the range of 0.43 to 42.64 µM. Only compound 4 exhibited antibacterial activity against Escherichisa coli, Bacillus subtilis, and Staphylococcus aureus (MIC 4.0, 2.0, and 4.0 µg/ml, respectively).

Libertellenones O-S and Eutypellenones A and B, Pimarane Diterpene Derivatives from the Arctic Fungus Eutypella sp. D-1.

Seven new pimarane-type diterpene derivatives, libertellenones O-S (1-5) and eutypellenones A and B (6 and 7), together with two known compounds (8 and 9), were isolated from the culture of Eutypella sp. D-1 obtained from high-latitude soil of the Arctic. Their structures were elucidated from spectroscopic data, as well as experimental and calculated electronic circular dichroism (ECD) analysis. Structurally, compounds 1-5 possess a cyclopropyl-fused pimarane diterpene moiety, whereas compounds 6 and 7 share an unusual cyclobutyl-fused pimarane diterpene skeleton. Compounds 1-9 exhibited cytotoxicities against HeLa, MCF-7, HCT-116, PANC-1, and SW1990 cells, with IC50 values in the range of 0.3 to 29.4 µM. Compounds 6 and 7 could dose-dependently inhibit the activity of NF-κB and exhibited significantly inhibitory effects on nitric oxide production induced by lipopolysaccharide.

Eutypellenoids A⁻C, New Pimarane Diterpenes from the Arctic Fungus Eutypella sp. D-1.

Three new pimarane diterpenes, eutypellenoids A⁻C (1⁻3), together with a known compound, eutypenoid C (4), were isolated from the culture extract of Eutypella sp. D-1 derived from the Arctic region. Compounds 1⁻3 possessed an uncommon tetrahydrofuran-fused pimarane diterpene skeleton. The structures of all compounds were determined by detailed spectroscopic analysis, electronic circular dichroism (ECD) analysis, as well as a comparison with the literature data. Antibacterial, antifungal, and cytotoxic activities of these compounds were evaluated. Compound 2 displayed antibacterial activity against Staphylococcus aureus and Escherichia coli with MIC values of 8 and 8 µg/mL, respectively. Additionally, compound 2 showed antifungal activity against Candidaparapsilosis, Candida albicans, Candida glabrata, and Candida tropicalis with MIC values of 8, 8, 16, and 32 µg/mL, respectively. Furthermore, compound 2 exhibited moderate cytotoxic activity against HCT-116 cell line with IC50 value of 3.7 µM.

Biotransformation of total coumarins of Radix Glehniae by Lecanicillium attenuatum W-1-9.

The biotransformation of total coumarins of Radix Glehniae by Lecanicillium attenuatum W-1-9 yielded three new products, lecaniside A (1), lecaniside B (2), and lecaniside C (3). The chemical structures of these metabolites were elucidated based on extensive spectral data, including 2D NMR and HRMS. The hydrogenation, dealkylation, glycosylation, and O-methylation reactions of these metabolites were observed in the present study. In the in vitro assays, compound 1 displayed a little PTP1B inhibitory activity.

Using a new plateau hyperbaric chamber to alleviate high altitude hypoxia: Rabbit and human studies.

OBJECTIVES: To validate the effects of the new plateau hyperbaric chamber on alleviating high altitude hypoxia on Mount Kun Lun. METHODS: A prospective, controlled study of rabbits and adult volunteers was conducted at altitudes of 355, 2880 and 4532m. We obtained arterial blood samples from rabbits and volunteers before and after hyperbaric treatment. The respiratory rate, heart rate, and blood pressure (BP) of adult volunteers were monitored during hyperbaric treatment. RESULTS: The mean PaO2 levels of experimental group rabbits and volunteers increased significantly after 60min of hyperbaric treatment at 350, 2880 and 4532m. The mean PaCO2 and pH levels of rabbits were not significant different before and after hyperbaric treatment at each altitude. The mean PaCO2 and pH levels were not significant different at 355m in the human study. However, at 2880 and 4532m, pH fell with increasing PaCO2 levels in humans before and after hyperbaric treatment. CONCLUSIONS: The new multiplace plateau hyperbaric chamber may be used to alleviate plateau hypoxia by increasing patient PaO2. However, its value in treating AMS must be confirmed in field conditions.

Development and preliminary test of a new plateau hyperbaric chamber.

OBJECTIVE: The objective of this study is to validate the performance, define its limits, and provide details on a new plateau hyperbaric chamber at 355-, 2880-, and 4532-m high altitude. METHODS: A new multiplace plateau hyperbaric chamber was designed to satisfy the needed of patients who have acute mountain sickness. Tests were conducted inside the chamber at 355-, 2880-, and 4532-m high altitude. The safely and conveniences of the new plateau hyperbaric chamber were estimated. RESULTS: Minimum pressures of the main compartment can reach up to 0.029, 0.022, and 0.02 MPa at 355-, 2880-, and 4532-m high altitude. During pressurization, there was no leak of air around the chamber. The time lag of pressure equilibration between main and buffer compartment varies from 30.3±2.01 to 200.5±5.44 seconds and between buffer compartment and ambient pressure varies from 60.2±4.13 to 215.9±6.76 seconds. CONCLUSIONS: The chamber can be applicated for acute mountain sickness treatment safety and convenience. However, further experience about animals and human within the chamber is needed to improve the hardware and establish conditions of effective utilization of this equipment in the high altitude.

Bioactive tyrosine-derived cytochalasins from fungus Eutypella sp. D-1.

Three new cytochalasins Z24 , Z25 , Z26 (1-3, resp.) and one known compound, scoparasin B (4), were isolated from the fungus Eutypella sp. D-1 isolated from the soil of high latitude of the Arctic. The structures of 1-3 were elucidated from spectroscopic data (NMR, MS). These compounds were evaluated for cytotoxic activities against several human tumor cell lines. Among them, compound 1 exhibited moderate cytotoxicity toward human breast cancer MCF-7 cell line with IC50 of 9.33 µM.

Disorders in angiogenesis and redox pathways are main factors contributing to the progression of rheumatoid arthritis: a comparative proteomics study.

OBJECTIVE: To clarify the pathogenesis of rheumatoid arthritis (RA) by comparing protein expression in fibroblast-like synoviocytes (FLS) from patients with RA with that in FLS from normal subjects, using proteomics analysis. METHODS: Proteins extracted from primary cultures of FLS obtained from 50 patients with RA and 10 normal subjects were analyzed by automated 2-dimensional nano-electrospray ionization liquid chromatography tandem mass spectometry. Differentially expressed proteins were screened by 2-sample t-test (P < 0.05) and fold change (>1.5), based on the bioinformatics analysis. The expression of vasculature development-related proteins (Thy-1, connective tissue growth factor [CTGF], and thrombospondin 1 [TSP-1]) and redox-related proteins (superoxide dismutase 2 [SOD2]) in synovial tissue was confirmed by real-time polymerase chain reaction and Western blotting. The effect of Thy-1 and CTGF knockdown on Thy-1, CTGF, TSP-1, and vascular endothelial growth factor (VEGF) was analyzed by RNA interference experiments. RESULTS: According to the criteria of having >1 unique peptide per protein present and a false discovery rate of ≤5%, 1,060 proteins were identified from patients with RA, and 1,292 proteins were identified from normal subjects, from which 100 differentially expressed proteins were screened out from the RA proteins. Of these, 46 proteins were up-regulated, and the remaining 54 proteins were down-regulated. Gene ontology and pathway analyses showed that 6 vasculature development-related proteins were up-regulated, including Thy-1, CTGF, and TSP-1, while 11 redox-related proteins were down-regulated, including SOD2. The results were consistent with those obtained using mass spectrometry. Thy-1, VEGF, CTGF, and TSP-1 were down-regulated after Thy-1 knockdown, and VEGF and CTGF were down-regulated after CTGF knockdown. Recombinant human CTGF could enhance proliferation and Transwell migration of human umbilical vein endothelial cells. CONCLUSION: Up-regulation of vasculature development-related proteins and down-regulation of redox-related proteins in FLS are predominant factors that may contribute to the pathogenesis of RA.

Cytotoxic meroterpenoids from the marine sponge Dactylospongia elegans.

Three new sesquiterpene quinones/hydroquinones, 20-demethoxy-20-isopentylaminodactyloquinone D (1), 20-demethoxy-20-isobutylaminodactyloquinone D (2), and 19-methoxy-dictyoceratin-A (3), and five known related compounds (4-8) were isolated from the marine sponge Dactylospongia elegans. Their structures were elucidated by spectroscopic analysis, ECD calculation, single-crystal X-ray diffraction, and comparison with the literature. Compounds 3 and 5-8 exhibited activities against the human cancer cell lines DU145, SW1990, Huh7, and PANC-1 with IC50 values ranging from 2.33 to 37.85 µM.

Rab11a and HSP90 regulate recycling of extracellular alpha-synuclein.

Growing evidence suggests that extracellular alpha-synuclein (eSNCA) may play an important role in the pathogenesis of Parkinson's disease (PD) and related synucleinopathies by producing neurotoxicity directly or via activation of glia. However, the mechanisms involved in the trafficking of eSNCA in neurons and/or glia remain unclear. Here, we demonstrated that eSNCA could be resecreted out of neurons via a process modulated by a recycling endosome regulator rab11a in addition to being degraded by an endosome-lysosome system. A quantitative proteomic analysis also revealed numerous proteins through which rab11a might execute its function. One of the candidate proteins, heat shock protein 90 (HSP90), was validated to be interacting with rab11a. Furthermore, geldanamycin, an HSP90 inhibitor, not only prevented resecretion of eSNCA but also attenuated neurotoxicity induced by eSNCA.

[Effects of vaporized perfluorocarbon therapy on seawater respiratory distress syndrome in rabbit models].

OBJECTIVE: To investigate the effects of vaporized perfluorocarbon therapy on pulmonary gas exchange and lung compliance in seawater respiratory distress syndrome rabbit models. METHODS: After induction of seawater respiratory distress syndrome by means of intratracheal injection of seawater, 24 female New Zealand rabbits were randomly divided into 3 groups: (1) CMV group (n = 8): Animals were ventilated with equal tidal volumes of 8 ml/kg during gas ventilation for 6 h. (2) PFC group (n = 8): For the first 2 h, animals received vaporized PFC with volumes of 6 - 7 mlxkg(-1)xh(-1), followed by gas ventilation for 4 h. (3) control group (n = 8): No ventilation was administered. Physiological and blood gas data were compared among the 3 groups by analysis of variance. The right lung of each animal was cut into 2 or 3 slides which were fixed with 10% buffered formalin for pathological evaluation. RESULTS: After lung injury, the measurements of lung compliance and oxygenation became significantly worse. After vaporized PFC for 30 min, lung compliance and oxygenation improved significantly as compared to the CMV group [(2 +/- 1) mm Hg/cm H2O vs (1 +/- 0) mm Hg/cm H2O (1 mm Hg = 0.133 kPa, 1 cm H2O = 0.098 kPa), F = 20, P < 0.05; (158 +/- 65) mm Hg vs (74 +/- 12) mm Hg, F = 26, P < 0.05]. After PFC inhalation, the improvement of oxygenation in PFC group lasted for 4 h [(253 +/- 96) mm Hg vs (78 +/- 19) mm Hg, F = 15, P < 0.05]. The lung injury score was also decreased in the PFC group compared to the CMV group (6.9 +/- 1.6 vs 9.8 +/- 1.3, chi(2) = 22, P < 0.05). All animals in the control group died in 15 min without ventilation. CONCLUSION: Vaporized PFC improved oxygenation and lung compliance and attenuated lung injury in a rat model of seawater induced respiratory distress syndrome.

[Effect of amygdalin on serum proteinic biomarker in pulmonary fibrosis of bleomycin-induced rat].

OBJECTIVE: To evaluate effect of amygdalin on expression of four biomarkers in the animal model of pulmonary fibrosis induced by bleomycin. METHODS: Rats were given one dose (5 mg/kg) of bleomycin in bleomycin-treated groups, amygdalin-treated groups and saline in controls by intratracheal instillation exposed surgically. The amygdalin-treated groups rats were treated with intraperitoneal injection of amygdalin (15 mg x kg(-1) x day(-1)). The rats were sacrificed 7, 14 and 28 days after bleomycin administration. Polarized light microscopy and Image-Pro Plus detected I and III collagen expressed in Paraffin-embedded lung sections stained with Sirius red. Surface-enhanced laser desorption-ionization time-of-flight mass spectrometry (SELDI-TOF MS) with weak cationic proteinchip (CM10) detected differentially expressed proteins in the pooled serum samples of all groups. RESULTS: Consistent fibrotic responses were found in all bleomycin and amygdalin-tread groups. On the 7th, 14th and 28th day after bleomycin or saline instillation, four differentially expressed proteins were detected in the pooled serum of all groups rats, consisting of 4 proteins with mass/charge ratio of 3530.7, 7043.5, 8332.6 and 9068.0, respectively. Compared with control groups, protein peaks intensity ratio with mass/charge ratio of 3530.7 on 7, 28 d and 7043.5, 8332.6 and 9068.0 on 7, 14 and 28 d was > 2 in bleomycin-treated groups. Compared with amygdalin-treated groups, protein peaks intensity with mass/charge ratio of 3530.7 at 7, 14, 28 d had no change almost, but protein peaks intensity ratio with mass/charge ratio of 7043.5 at 7 d, 8332.6 on 28 d and 9068.0 on 14 d was > 2 in bleomycin-tread groups. All the four protein peaks intensity had no change almost at other point. CONCLUSION: Amygdalin may reduce the bleomycin-induced increase of differentially expressed protein peak intensities in rat serum.

[Effects of positive end expiratory pressure ventilation upon respiratory function and hydrophobic surfactants proteins in rabbit with seawater respiratory distress syndrome].

OBJECTIVE: To investigate the effects of positive end-expiratory pressure (PEEP) ventilation upon respiratory function and lung surfactant protein B (SP-B)/SP-C in seawater respiratory distress syndrome (SW-RDS) rabbit. METHODS: Twenty-four female New Zealand rabbits were randomly equally divided into three groups:conventional mechanical ventilation (CMV) group, PEEP group, and control group. After anesthesia and tracheal intubation followed by 20 minutes of CMV, SW-RDS model was established by lung perfusion of artificial seawater through tracheal intubation. Then the CMV group ventilated for 6 hours (each parameter unchanged); PEEP group ventilated with PEEP of 8 cm H2O for 2 hours based on prior parameters and subsequently with CMV for 4 hours; control group without ventilation after modeling. Oxygenation indices and lung compliance were continuously monitored during ventilation. After ventilation, the rabbits in study groups were sacrificed while those dying a natural death in the control group selected. Bronchoalveolar lavage fluid of the left lung was collected to determine the alveolar surface tension and the right lung was harvested to measure the mRNA expression of SP-B/SP-C by real-time PCR as well as SP-B protein by Western blotting. RESULTS: After modeling, the data of lung compliance and oxygenation indices became significantly worse in every group but without statistical difference in three groups. All rabbits in control group died within 15 minutes of ventilator withdrawal. After receiving PEEP ventilation for 30 minutes, these indices significantly improved compared with CMV group in which there was no significant change of the indices (P < 0.05). Minimal alveolar surface tension in CMV group (mN/m, 30.8 +/- 6.3) was greater than in PEEP group (21.1 +/- 4.4, P < 0.05) and control group (23.6 +/- 4.6, P < 0.05); SP-B/SP-C mRNA relative expression (0.37 +/- 0.15/0.60 +/- 0.19) and SP-B relative protein abundance (0.38 +/- 0.17) in CMV group were obviously lower than in PEEP group (0.73 +/- 0.15/0.92 +/- 0.40, 0.52 +/- 0.22, P < 0.05). CONCLUSIONS: PEEP ventilation can improve the oxygenation indices and lung compliance in SW-RDS animals. And such an effect is correlated with both the mRNA expressions of SP-B/SP-C and mechanical distension.

MicroRNA-422a functions as a tumor suppressor in non-small cell lung cancer through SULF2-mediated TGF-ß/SMAD signaling pathway.

MicroRNAs (miRNAs) have been demonstrated to participate in a variety of human cancers by functioning as post-transcriptional regulators of oncogenes or antioncogenes including non-small cell lung cancer (NSCLC). The aim of the current study was to identify the role of miR-422a in NSCLC via sulfatase 2 (SULF2) to further elucidate the mechanism of NSCLC. Initially, the expression of miR-422a and SULF2 was determined in NSCLC tissues and cells. The role of miR-422a in NSCLC was identified in relation with a miR-422a mimic or inhibitor, siRNA against SULF2 and TGF-ß1. The regulatory effects of miR-422a were examined following detection of the related epithelial mesenchymal transition (EMT)-related genes, and the apoptosis-related genes and evaluation of their cellular biological functions. The expression pattern of miR-422a, SULF2, and the TGF-ß/SMAD pathway-related genes was detected to elucidate the mechanism by which miR-422a influences the progression of NSCLC. Finally, xenograft tumors in nude mice were observed for tumorigenicity evaluation purposes. Our results showed that miR-422a was poorly expressed while SULF2 was highly expressed in NSCLC. Dual luciferase reporter gene assay further verified that miR-422a targeted SULF2. Altogether, this study demonstrated that miR-422a downregulated SULF2 to inhibit the TGF-ß/SMAD pathway. NSCLC cell proliferation, migration, invasion, colony formation, EMT and tumorigenesis were all inhibited while apoptosis was promoted upon restoration of miR-422a or silencing of SULF2. However, the activation of the TGF-ß/SMAD pathway was determined to reverse the tumor-suppressive effects of si-SULF2. miR-422a restoration, which ultimately inhibited the progression of NSCLC by suppressing the TGF-ß/SMAD pathway via SULF2.

Surgical treatment ofpatients with severe non-flail chest rib fractures.

BACKGROUND: Many patients have inadequate long-term analgesia, respiratory distress, and hypoxemia due to a long-standing substantial smoking history or the presence of primary pulmonary diseases; analgesic treatment is not valid in these patients. Even if the imaging findings of rib fractures are relatively mild, rib fractures may cause severe position limitation, respiratory distress, and hypoxemia. AIM: To investigate the curative effect of surgical treatment for patients with severe non-flail chest rib fractures. METHODS: A total of 78 patients from our hospital with severe noncontinuous thoracic rib fractures from September 2016 to September 2018 were enrolled in our study. Thirty-nine patients underwent surgical treatment, and 39 underwent conservative treatment. The surgical treatment group received surgery performed with titanium plates, and the screws were inserted with open reduction and internal fixation. The conservative treatment group received analgesia and symptomatic treatment. The pain scores at 72 h, 1 wk, 2 wk, 4 wk, 6 wk, 3 mo, and 6 mo were compared, and the SF-36 quality of life scores were compared atthe 3rd and 6th months. RESULTS: Pain relief in the surgical group was significantly better than that in the conservative group at each time point (72 h, 1 wk, 2 wk, 4 wk, 6 wk, 3 mo, and 6 mo after surgery, P < 0.001). ( The SF-36 scores were significantly higher in the surgical group than in the conservative group at 1 mo and 6 mo (P < 0.05). CONCLUSION: Patients with severe non-flail chest rib fractures have a better quality of life following surgical treatment than following conservative treatment, and surgical treatment is also useful for relieving pain. We should pay more attention to the physiological functions and clinical manifestations of patients with severe rib fractures. In patients with non-flail chest rib fractures, surgical treatment is feasible and effective.

[The preventive effects of intraperitoneal injection of perfluorocarbon on acute lung injury in rat].

OBJECTIVE: To evaluate the preventive effects of intraperitoneal injection of perfluorocarbon (PFC) on acute lung injury (ALI) in rat. METHODS: Sixty-three male Wistar rats were randomly divided into normal control (NC) group, lipopolysaccharide (LPS) group and C8F18 group. Rats in NC group were sacrificed 2 hours after anesthesia, and in LPS group and C8F18 group rats were either treated with normal saline or C8F18 15 ml/kg intraperitoneally 48 hours before LPS challenge. ALI was reproduced by intravenous injection of 7 ml/kg LPS, and the extent of lung injury was assessed by arterial partial pressure of oxygen (PaO(2)) level, histological examination, right lung wet weight/body weight (W/D) ratio, tumor necrosis factor-alpha (TNF-alpha) level in serum and broncho alveolar lavage fluid (BALF) at 2, 4, 6 hours after injury. RESULTS: PaO(2) in LPS group and C8F18 group was significant lower than that in NC group (both P<0.05). There were no difference in PaO(2) between LPS group and C8F18 group at 2, 4, 6 hours after injury (all P>0.05). Compared with NC group, TNF-alpha level in blood and BALF increased obviously in LPS group and C8F18 group (both P<0.05). There was no significant change in content of TNF-alpha in C8F18 group BALF at 6 hours was significantly lower than that in LPS group (P<0.05). CONCLUSION: Intraperitoneal administration of C8F18 (15 ml/kg) can not attenuate pathological changes or improve PaO(2) in rats with ALI induced by LPS in a short time.

[Effect of Na(+)/Ca(2+) exchange blocker, Benzamil, on alveolar macrophage function in patients with chronic obstructive pulmonary disease].

OBJECTIVE: To observe the effect of Benzamil on cytosolic free calcium ions ([Ca(2+)] i) concentration, tumor necrosis factor-alpha (TNF-alpha) and malondialdehyde (MDA) in alveolar macrophage (AM) in patients with chronic obstructive pulmonary disease (COPD). METHODS: Alveolar macrophages were collected from bronchoalveolar lavage fluid, and they were cultured and [Ca(2+)] i were determined by calcium fluorescent with indicator Fura-2/AM. The effects of Benzamil on the increase in cytosolic [Ca(2+)] i and on secretion of TNF-alpha, MDA were investigated in 36 patients with COPD and 36 healthy volunteers. RESULTS: (1) [Ca(2+)] i concentration (68.26+/-7.24) nmol/L, TNF-alpha (5.74+/-0.42) ng/L and MDA (3.77+/-0.61) microg/L were found in COPD patients, and they were significantly increased, as compared with the control group, in whom the contents were [Ca(2+)] i concentration (60.61+/-6.26) nmol/L, TNF-alpha (2.06+/-0.20) microg/L, MDA (1.91+/-0.19) ng/L (all P<0.01). (2)The following data namely [Ca(2+)] i concentration (168.34+/-17.58) nmol/L, TNF-alpha (9.67+/-1.01) ng/L and MDA (11.21+/-1.01) microg/L were obtained after anoxia in COPD patients (all P<0.01). (3)After incubation with Benzamil, and then subjected the cells to anoxia, the following data were obtained: [Ca(2+)] i concentration (129.21+/-14.33) nmol/L, TNF-alpha content (6.78+/-0.52) ng/L and MDA (8.47+/-0.79) microg/L and they were all lower than only anoxia was applied (all P<0.01). CONCLUSION: Benzamil not only downregulates alveolar macrophages activity but also suppresses the generation of the TNF-alpha and MDA.

A new sesquiterpene lactone from fungus Eutypella sp. D-1.

We isolated and identified a new sesquiterpene lactone which we named eut-Guaiane sesquiterpene (1), along with four cytochalasins from the fungus Eutypella sp. derived from the soil of high latitude of Arctic. The new structure was determined by spectroscopic studies such as 1D and 2D NMR and MS analyses, while the known compounds were identified by comparison of the NMR data with those in literatures. New compound 1 exhibited strong antibacterial activity against Escherichia coli, Bacillus subtilis and Staphylococcus aureus. Besides, it showed a little cytotoxicity against SGC7901 cell line.