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Six new xanthone dimers, diaporxanthones A-F (1-6), and an unusual xanthone monomer diaporxanthone G (7), in addition to seven known analogues (8-14), were isolated and identified from endophytic Diaporthe goulteri L17 harbored in the fruits of the salt-tolerant plant Vitex trifolia. The chemical structures of these metabolites were elucidated on the basis of nuclear magnetic resonance, high-resolution electrospray ionization mass spectrometry, and reported data in the literature. Their absolute configurations were established by single-crystal X-ray diffraction analysis together with time-dependent density functional theory electronic circular dichroism calculations. Among these compounds, compounds 1 and 6 exhibited moderate antifungal activities against Nectria sp. and Colletotrichum musae and compound 4 showed significant cytotoxicity against all selected five cancer cell lines.

Fusidic acid, a representative member of fungal fusidane triterpenoids, has been clinically used as an antibiotic. In the present study, fusidic acid (1), and its known analogs 16-desacetylfusidic acid (2) and 3β,20-dihydroxy-protosta-16,24-dien-29-oic acid (4), together with one new derivative acremonidiol A (3), were isolated from the endophytic fungus, Acremonium pilosum F47. Their structures were determined by MS and NMR. The spectroscopic data of 2 are firstly reported here. The antibacterial efficacies of 1-4 were evaluated against four selected Gram-positive or Gram-negative bacteria. As expected, only compound 1 showed strong inhibitory effect on Gram-positive bacteria Staphylococcus aureus and Bacillus subtilis.

Three zinniol analogues, pleoniols A–C (1–3), together with a known compound (4), were isolated from a mixed fermentation of two endophytic fungi, Pleosporales sp. F46 and Acremonium pilosum F47, both of which are found the pedicel of the medicinal plant Mahonia fortunei. High-performance liquid chromatography analysis showed that none of compounds 1–4 were detected when either one of the two fungi was cultured alone. The structures of compounds 1–4, including the absolute configurations, were deduced based on the interpretation of HRMS, NMR, and optical rotation data. Compounds 1–3 exhibited no antimicrobial efficacies against four Gram-positive or Gram-negative bacteria and two plant pathogenic fungi. Moreover, they demonstrated no obvious cytotoxic activities against four cancer cell lines, A549, MDA-MB-231, CT-26 and MCF-7. Our work indicates that the co-culture of endophytes in the same ecological niche is an effective approach for promoting interspecies interaction and enriching chemical diversity.

Three new sorbicillinoids, including trimer trisorbicillinone E (

Two new heptaketides, pleosporalins H and I (1 and 2), as well as seven biosynthetically related known polyketides (3–9) were isolated from the endophytic fungus, Pleosporales sp. F46 by employing ...

Bevacizumab (BVZ) is the first recombinant humanized monoclonal antibody against vascular endothelial growth factor (VEGFA) approved by the FDA for the treatment of different kinds of cancers, especially colorectal cancer. Although the anti-tumor effects have been verified, the side effects of BVZ are also noteworthy, among which, cardiotoxicity may be the most serious side effect of BVZ. However, the exact mechanisms of cardiotoxicity induced by BVZ have been little explored. This study was conducted in vitro in a human cardiac myocyte (HCM) model. MTT assay was conducted to determine BVZ-stimulated cell viability. For testing the function and mechanism, the cells were transfected with miR-140-5p mimics, miR-140-5p inhibitor and/or VEGFA small interfering RNA (si-VEGFA). Then, apoptosis of the cells was detected via annexin V/propidium iodide (AV-PI) staining followed by flow cytometry. qRT-PCR and western blot assays were applied to measure gene expression (i.e. mRNA) and protein levels, respectively. The CK, LDH, SOD, CAT and GSH-Px activities and MDA level were determined using commercial kits. ROS levels were determined by DCFH-DA assay. Mitochondrial membrane potential was measured by JC-1 assay. Dual-luciferase reporter assay was used to detect the interaction between miR-140-5p and VEGFA. BVZ could inhibit HCM proliferation and induce apoptosis. miR-140-5p was upregulated in response to BVZ treatment and miR-140-5p restraint could alleviate HCM damage caused by BVZ treatment. In contrast, VEGFA and 14-3-3γ expressions were down-regulated by BVZ, and miR-140-5p could inhibit the expression of 14-3-3γ by directly targeting VEGFA. Moreover, VEGFA suppression enhanced HCM injury stimulated by BVZ and partially reversed the functional role of the miR-140-5p inhibitor in BVZ-treated cells. Taken together, miR-140-5p promoted BVZ-treated cardiomyocyte toxicity by targeting the VEGFA/14-3-3γ signal pathway. Collectively, miR-140-5p mediated the BVZ-induced cytotoxicity to cardiomyocytes by targeting the VEGFA/14-3-3γ signal pathway, indicating that miR-140-5p may be a novel target for treating BVZ-induced cardiotoxicity.

Chamiside A (1), a novel cytochalasan with a new 6/6/5-fused tricyclic core skeleton, was isolated from an endophytic fungus, Chaetomium nigricolor F5, harbored in the medicinal plant Mahonia fortunei. Its structure was unambiguously determined by extensive spectroscopic analyses, measurement of single-crystal X-ray diffraction, and electronic circular dichroism calculation. A biosynthetic pathway for the unique ring system in 1 was proposed. Compound 1 exhibited moderate antibacterial activity against Staphylococcus aureus.

Myotonic dystrophy (DM) is a genetic disorder featured by muscular dystrophy. It is caused by CUG expansion in the myotonic dystrophy protein kinase gene that leads to aberrant signaling and impaired myocyte differentiation. Many studies have shown that microRNAs are involved in the differentiation process of myoblasts. The purpose of this study was to investigate how the miR-322/miR-503 cluster regulates intracellular signaling to affect cell differentiation. The cell model of DM1 was employed by expressing GFP-CUG200 or CUGBP Elav-like family member 1 (Celf1) in myoblasts. Immunostaining of MF-20 was performed to examine myocyte differentiation. qRT-PCR and western blot were used to determine the levels of Celf1, MyoD, MyoG, Mef2c, miR-322/miR-503, and mitogen-activated protein kinase/extracellular signal-regulated kinase (MEK/ERK) signaling. Dual luciferase assay was performed to validate the interaction between miR-322/miR-503 and Celf1. CUG expansion in myoblasts impaired the cell differentiation, increased the Celf1 level, but it decreased the miR-322/miR-503 levels. miR-322/miR-503 mimics restored the impaired differentiation caused by CUG expansion, while miR-322/miR-503 inhibitors further suppressed. miR-322/miR-503 directly targeted Celf1 and negatively regulated its expression. Knockdown of Celf1 promoted myocyte differentiation. Further, miR-322/miR-503 mimics rescued the impaired differentiation of myocytes caused by CUG expansion or Celf1 overexpression through suppressing of MEK/ERK signaling. miR-322/miR-503 cluster recover the defective myocyte differentiation caused by RNA-toxic via targeting Celf1. Restoring miR-322/miR-503 levels could be an avenue for DM1 therapy.

A new γ-pyrone derivative, acrepyrone A (1), and three known sorbicillinoids, trichodimerol (2), dihydrotrichodimerol (3) and tetrahydrotrichodimerol (4) were isolated from an endophytic fungus, Acremonium citrinum SS-g13, harboured in the roots of the Chinese medicinal plant Fructus mori. Their structures were determined by analysing MS, NMR, and ECD data. Compound 1 was evaluated for its cytotoxic effect, antibacterial activity and quorum sensing inhibitory potential.

Two new α-pyrones, fupyrones A and B (1 and 2) and a biosynthetically related known α-pyrone, 4-methyl-5,6-dihydro-2H-pyran-2-one (3), were isolated from an endophytic fungus, Fusarium sp. F20, harbored in the stems of the Chinese medicinal plant Mahonia fortunei. Their structures were determined on the basis of spectroscopic data including MS and NMR. The antibacterial efficacies of compounds 1-3 were evaluated against four selected Gram-positive and Gram-negative bacteria, and their quorum sensing inhibitory activity was also investigated against the test organism, Chromobacterium violaceum.

Six new heptaketides, pleosporalins A–F (1–5, and 7), and a new heptaketide derivative, pleosporalin G (9), together with four biosynthetically related known compounds (6, 8, 10, and 11), were isolated from an endophytic fungus, Pleosporales sp. F46, found in the medicinal plant Mahonia fortunei. The structures and stereochemistry of these compounds were established by extensive spectroscopic analyses including LC-HRMS, NMR spectroscopy, optical rotations, ECD calculations, and single-crystal X-ray diffraction. The antifungal activities of isolated compounds 1–11 were investigated against Candida albicans, and their cytotoxic activities were evaluated against A549, SMMC-721, and MDA-MB-231 cancer cell lines. Compound 1 was active against C. albicans with an MIC80 of 128 μg mL−1, and compound 7 showed moderate cytotoxicity against MDA-MB-231 with an IC50 of 22.4 ± 1.1 μM. By comparing compounds 1 and 7 with structurally related metabolites, it was revealed that alterations to their C-1 or C-2 substitutions could significantly influence their antifungal or cytotoxic efficacies.

Two new heptaketides, pleosporalins H and I (

Bevacizumab (BVZ) is the first recombinant humanized monoclonal antibody against vascular endothelial growth factor (VEGFA) approved by the FDA for the treatment of different kinds of cancers, especially colorectal cancer. Although the anti-tumor effects have been verified, the side effects of BVZ are also noteworthy, among which, cardiotoxicity may be the most serious side effect of BVZ. However, the exact mechanisms of cardiotoxicity induced by BVZ have been little explored. This study was conducted in vitro in a human cardiac myocyte (HCM) model. MTT assay was conducted to determine BVZ-stimulated cell viability. For testing the function and mechanism, the cells were transfected with miR-140-5p mimics, miR-140-5p inhibitor and/or VEGFA small interfering RNA (si-VEGFA). Then, apoptosis of the cells was detected via annexin V/propidium iodide (AV-PI) staining followed by flow cytometry. qRT-PCR and western blot assays were applied to measure gene expression (i.e. mRNA) and protein levels, respectively. The CK, LDH, SOD, CAT and GSH-Px activities and MDA level were determined using commercial kits. ROS levels were determined by DCFH-DA assay. Mitochondrial membrane potential was measured by JC-1 assay. Dual-luciferase reporter assay was used to detect the interaction between miR-140-5p and VEGFA. BVZ could inhibit HCM proliferation and induce apoptosis. miR-140-5p was upregulated in response to BVZ treatment and miR-140-5p restraint could alleviate HCM damage caused by BVZ treatment. In contrast, VEGFA and 14-3-3γ expressions were down-regulated by BVZ, and miR-140-5p could inhibit the expression of 14-3-3γ by directly targeting VEGFA. Moreover, VEGFA suppression enhanced HCM injury stimulated by BVZ and partially reversed the functional role of the miR-140-5p inhibitor in BVZ-treated cells. Taken together, miR-140-5p promoted BVZ-treated cardiomyocyte toxicity by targeting the VEGFA/14-3-3γ signal pathway. Collectively, miR-140-5p mediated the BVZ-induced cytotoxicity to cardiomyocytes by targeting the VEGFA/14-3-3γ signal pathway, indicating that miR-140-5p may be a novel target for treating BVZ-induced cardiotoxicity.

Six new heptaketides, pleosporalins A-F (1-5, and 7), and a new heptaketide derivative, pleosporalin G (9), together with four biosynthetically related known compounds (6, 8, 10, and 11), were isolated from an endophytic fungus

Azole antifungals are commonly used to treat fungal infections but have resulted in the occurrence of drug resistance. Therefore, developing azole derivatives (AZDs) that can both combat established drug-resistant fungal strains and evade drug resistance is of great importance. In this study, we synthesized a series of AZDs with a fluconazole (FLC) skeleton conjugated with a mitochondria-targeting triphenylphosphonium cation (TPP+). These AZDs displayed potent activity against both azole-sensitive and azole-resistant Candida strains without eliciting obvious resistance. Moreover, two representative AZDs, 20 and 25, exerted synergistic antifungal activity with Hsp90 inhibitors against C. albicans strains resistant to the combination treatment of FLC and Hsp90 inhibitors. AZD 25, which had minimal cytotoxicity, was effective in preventing C. albicans biofilm formation. Mechanistic investigation revealed that AZD 25 inhibited the biosynthesis of the fungal membrane component ergosterol and interfered with mitochondrial function. Our findings provide an alternative approach to address fungal resistance problems.

A new

Myocardial ischemia-reperfusion (I/R) is a common and lethal disease that threatens people’s life worldwide. The underlying mechanisms are under intensive study and yet remain unclear. Here, we explored the function of miR-322/503 in myocardial I/R injury. We used isolated rat perfused heart as an in vivo model and H9c2 cells subjected with the oxygen and glucose deprivation followed by reperfusion as in vitro model to study myocardial I/R injury. 2,3,5-Triphenyltetrazolium chloride (TTC) staining was used to measure the infarct size, and terminal deoxynucleotidyl transferase dUTP-mediated nick-end label (TUNEL) staining was used to examine apoptosis. Quantitative RT-PCR and Western blot were used to determine expression levels of miR-322/503, Smad ubiquitin regulatory factor 2 (Smurf2), enhancer of zeste homolog 2 (EZH2), p-Akt, and p-GSK3β. Overexpression of miR-322/503 decreased infarct size, inhibited cell apoptosis, and promoted cell proliferation through upregualtion of p-Akt and p-GSK3β. Thus the expression of miR-322/503 was reduced during I/R process. On the molecular level, miR-322/503 directly bound Smurf2 mRNA and suppressed its translation. Smurf2 ubiquitinated EZH2 and degraded EZH2, which could activate Akt/GSK3β signaling. Our study demonstrates that miR-322/503 plays a beneficial role in myocardial I/R injury. By inhibition of Smurf2 translation, miR-322/503 induces EZH2 expression and activates Akt/GSK3β pathway, thereby protecting cells from ischemia reperfusion injury.

A new ergosterol derivative, 23R-hydroxy-(20Z,24R)-ergosta-4,6,8(14),20(22)-tetraen-3-one (1), and a biosynthetically related known compound, (22E,24R)-ergosta-4,6,8(14),22-tetraen-3-one (2), were isolated from the co-culture between endophytic fungus Pleosporales sp. F46 and endophytic bacterium Bacillus wiedmannii Com1 both inhibiting in the medicinal plant Mahonia fortunei. The structure of the new compound 1 was determined by extensive spectroscopic analysis using HRMS and NMR, together with the modified Mosher's ester method. This is the first example of isolation of a ergosterol derivative with a Δ20(22)-double bond in the side chain. Compound 1 exhibited moderate antibacterial efficacy against Staphylococcus aureus and no obvious cytotoxic activities against the cancer cell lines A549, MDA-MB-231 and Hct116. Our results not only reveal that compound 1 is a potent antibacterial lead compound, but also highlight the powder of co-cultivation for inducing the production of cryptic natural products from endophytes derived from the same host plant.

Objectives: In this study, we aim to determine how CUG-expansion and the abundance of Celf1 regulates normal myocyte differentiation and reveal the role ofmiR-206 in myotonic dystrohy and explore a possible gene therapy vector. Methods: we set up CUG-expansion and Celf1 overexpression C2C12 cell models to imitate the myocyte differentiation defects of DM1, then transfected AdvmiR-206 into cell models, tested the level of myogenic markers MyoD, MyoG, Mef2c, Celf1 by RT-PCRand Western Blotting, detected myotube formation by myosin heavy chain immunostaining. Result: 3'-UTR CUG-expansion leads to myotube defects and impaired myoblasts differentiation. Overexpression of Celf1 inhibits myoblast differentiation and impairs differentiation. Knockdown of Celf1 partially rescues differentiation defects of myoblasts harboring CUG-expansion. miR-206 incompletely reverses myoblast differentiation inhibition induced by CUG-expansion and partially recuses myoblast differentiation defects induced by Celf1 overexpression. Conclusions: Ectopic miR-206 mimicking the endogenous temporal patterns specifically drives a myocyte program that boosts myoblast lineages, likely by promoting the expression of MyoD to rectify the myogenic deficiency by stimulating the accumulation of Celf1. Abbreviations: DMPK: (dystrophia myotonica protein kinase); 3'-UTR: (3'-untranslated region); MBNL1: (muscleblind-like [Drosophila]); DM1: (myotonic dystrophy type 1); GFP: (green fluorescent protein); RT-PCR: (quantitative reverse transcriptase-polymerase chain reaction); shRNA: (short hairpin RNA).

lipid metabolism is the major causes of atherosclerosis. There is increasing evidence that miR-133a plays an important role in atherosclerosis. However, the regulatory mechanism of miR-133a in macrophages is still unclear. Several lines of evidence indicate that loss of TR4 leads to reduce lipid accumulation in liver and adipose tissues, etc, and lesional macrophages-derived TR4 can greatly increase the foam cell formation through increasing the CD36-mediated the uptake of ox-LDL. Interestingly, computational analysis suggests that TR4 may be a target gene of miR-133a. Here, we examined whether miR-133a regulates TR4 expression in ox-LDL-induced mouse RAW 264.7 macrophages, thereby affecting lipid accumulation. Using ox-LDL-treatment RAW 264.7 macrophages transfected with miR-133a mimics or inhibitors, we have showed that miR-133a can directly regulate the expression of TR4 in RAW 264.7 cells, thereby attenuates CD36-medide lipid accumulation. Furthermore, our studies suggest an additional explanation for the regulatory mechanism of miR-133a regulation to its functional target, TR4 in RAW 264.7 macrophages. Thus, our findings suggest that miR-133a may regulate lipid accumulation in ox-LDL-stimulated RAW 264.7 macrophages via TR4-CD36 pathway.

The aim of the present study was to investigate whether oxidative stress and immune dysfunction could be attenuated by Ganoderma atrum polysaccharide (PSG-1) in d-galactose (d-gal)-induced aging mice, and provide evidence for its effects. The results showed that PSG-1 significantly decreased lipid peroxidation in liver, brain, and spleen, but concomitantly increased the activities of superoxide dismutase, catalase, and glutathione peroxidase compared with the d-gal group. Elevation of glutathione contents and attenuation of glutathione disulfide contents were also found in PSG-1-treated animals. Furthermore, the results showed that PSG-1 treatment increased basal lymphocyte proliferation as well as T cell and B cell proliferation and enhanced interleukin-2 production. Taken together, the results suggested that PSG-1 had potential as a novel agent to promote health and improve aging-associated pathologies, at least in part, via modification of the redox system and improvement of immune function.

A new cyclopentanopyridine alkaloid, 3-hydroxy-5-methyl-5,6-dihydro-7H-cyclopenta[b]pyridin-7-one (1), together with 11 known aromatic compounds were isolated from the secondary metabolites of the halotolerant fungal strain Wallemia sebi PXP-89 in 10% NaCl. Their structures including the absolute configurations of (2S,3S)-1-(4-hydroxyphenyl)butane-2,3-diol (2), (2R,3S)-1-(4-hydroxyphenyl)butane-2,3-diol (3), and (S)-3-hydroxy-4-(4-hydroxyphenyl)-2-one (4) were elucidated by spectroscopic analysis and a modified Mosher's method. Compound 1 exhibited antimicrobial activity against Enterobacter aerogenes with a MIC of 76.7 μM. The absolute configurations of compounds 2-4 were determined for the first time.

Cytokeratin 19 fragment antigen 21-1 (CYFRA21-1) can be used for the quantitative examination of fragment of cytokeratin 19, and is a valuable tumor marker in various malignancies. This study was to investigate the significance of pretreatment serum CYFRA21-1 and squamous cell carcinoma antigen (SCCAg) in diagnosis and their correlations to the clinicopathologic features of cervical carcinoma.One hundred cervical carcinoma patients underwent pretreatment serum CYFRA21-1 and SCCAg evaluation; 20 healthy women were subjected as control. The specificity and sensitivity of CYFRA21-1 and SCCAg as diagnostic indexes were analyzed; their correlations to clinicopathologic features were investigated through univariate and multivariate analyses.The specificity of CYFRA21-1 and SCCAg in diagnosing cervical cancer were both 100%. The sensitivity of CYFRA21-1 and SCCAg in diagnosing cervical cancer were 36.0% and 47.0% respectively, without significant difference. The combined examination of CYFRA21-1 and SCCAg elevated the sensitivity to 60.0%, which was significantly higher than that of examining CYFRA21-1 alone. Univariate analysis showed elevation of CYFRA21-1 was related with FIGO stage and tumor size; elevation of SCCAg was related with pathologic type, tumor size, deep stromal invasion and pelvic node metastasis. Multivariate analysis showed that elevation of CYFRA21-1 had no relationship with any factors, while elevation of SCCAg was related with deep stromal invasion and pelvic node metastasis. The sensitivity of SCCAg in predicting pelvic node metastasis and deep stromal invasion were significantly higher than those of CYFRA21-1 (75.0% vs. 29.2%, p = 0.001; 55.8% vs. 26.9%, p = 0.024), and the addition of CYFRA21-1 to SCCAg could not significantly improve the sensitivity compared with SCCAg alone (79.2% vs. 75.0%, p0.05; 63.5% vs. 55.8%, p0.05).The value of pretreatment serum CYFRA21-1 as predictor of pelvic node metastasis and deep stromal invasion is less significant compared with that of SCCAg. For cervical squamous cell cancer, SCCAg is the preferred tumor marker.

To investigate the effects of Xuezhikang (XZK) on serum levels of high sensitivity-C reactive protein (Hs-CRP), matrix metalloproteinase-9 (MMP-9) and lipoprotein in patients with acute coronary syndrome (ACS).Sixty-nine ACS patients were divided into the XZK group (40 cases) treated with conventional therapy and XZK and the control group (29 cases) with conventional therapy alone, another 30 healthy persons were assigned as the normal group. Before and after the treatment, the levels of Hs-CRP, MMP-9 and lipids were detected.Compared with those in the normal subjects, Hs-CRP and MMP-9 levels in the ACS patients increased significantly (P0.05), parallel with the extent of myocardial injury. After 2 weeks of XZK treatment, levels of Hs-CRP and MMP-9 of the XZK group decreased significantly (P0.05), while lipids levels had no remarkable changes.Hs-CRP and MMP-9 levels were closely correlated to the genesis and severity of ACS. Anti-inflammatory action of XZK plays an important role in early stage treatment of ACS patients.

Advanced ovarian cancer shows a high recurrence and poor survival rate. It is important to identify the risk factors for the recurrence of ovarian cancer, due to the lack of reliable methods for the detection of early disease. This study was designed to explore the risk factors for the recurrence of epithelial ovarian cancer.Factors that might be related to the recurrence of 109 epithelial ovarian cancer patients including age, pathological type, FIGO stage, operation type, chemotherapy regimen, neoadjuvant chemotherapy, postoperative chemotherapy cycles, first operation status, and size of residual tumor were analyzed by logistic regression model using SPSS 10.0 statistical software.Of 109 patients with ovarian cancer, 36 (33%) relapsed after a combination of surgery and chemotherapy, and the median recurrence-free interval was 19 months. The 5-year survival rates were 62.7% and 43.3% for the 109 patients and the recurrent patients, respectively. The survival rates of pelvic recurrence (50.1%) and extra-pelvic recurrence (36.1%) were not statistically different. Univariate analysis showed that the risk of recurrence in mucous adenocarcinoma or FIGO stage I patients were lower than that of other pathology type or FIGO stage (beta=-1.565 and -1.799,P=0.0120 and 0.026 ) while it was higher in the patients given above 8 cycles chemotherapy than those given 1-4 or 6-8 cycles(beta=-3.591 and -1.500,P0.001 and =0.038). Multivariate analysis showed that histological type, FIGO stage and postoperative chemotherapy cycles had remarkable influence on the relapse of epithelial ovarian cancer independently(RR=3.473, 4.713, and 6.140, respectively, P0.05).Histological type, FIGO stage, and postoperative chemotherapy cycles influence the recurrence of epithelial ovarian cancer. Since FIGO stage is a remarkable risk factor for the recurrence, early diagnosis should be the key point to decrease it. Reasonable chemotherapy plan is essential for the therapy of ovarian cancer, but excessive chemotherapy is not good for effectiveness.

Experimental and clinical evidence links tumor growth, invasion, and metastatic potential with neoangiogenesis. This process is modulated by several angiogenic growth factors, such as vascular endothelial growth factor(VEGF). Few data are currently available on serum level in patients with gynaecological malignant tumors. This study was designed to determine the serum VEGF level in the patients with gynaecological malignant tumors and its significance as a tumor marker.Preoperative serum VEGF level were measured in 50 cervical cancer, 39 endometrial cancer, 89 ovarian cancer patients, and 80 normal healthy women; The serum VEGF levels were also measured in 3, 6, 9 months after operation and when recurrence in three curative resection patients with ovarian cancer; using commercially available enzymelinked immonosarbent assay (RD systems Inc. Minneapolis, MN, USA). Statistical analysis was performed by using the SPSS9.0 software package. Using 5th and 95th percentage describe the variant degree.The median level of VEGF in sera of 80 healthy women was 218.50 ng/L(42.06-671.70 ng/L), while in 50 cervical cancer, 39 endometrial cancer, and 89 ovarian cancer patients were 272.00 ng/L(91.94-745.53 ng/L), 383.50 ng/L(105.67-776.50 ng/L), and 479.85 ng/L (99.47-1326.88 ng/L), respectively. The VEGF levels in endometrial cancer and ovarian cancer patients were significantly higher than that in healthy women (P0.0001). But in cervical cancer patients the VEGF level, was not significant diffent compare with health wanen. After operation, 3, 6, 9 months the VEGF levels in 3 ovarian cancer patients were significantly lower than that of preoperative but it ascended again when the disease was recurrent 14, 17 months later in two cases. The VEGF level was significantly higher in advanced ovarian cancer patients (stage III-IV) than that in the early stage (stage I-II) (P0.05).The serum level of the VEGF may be used as a new tumor marker of endometrial cancer and ovarian cancer, for diagnoses and monitoring the progress of the disease.

The title ergosterol compound, C(28)H(44)O(4)·H(2)O, is composed of four fused rings (three six-membered and one five-membered) and a side chain. It is a derivative of ergosterol and was isolated from a marine-derived halotolerant fungus, Cladosporium cladosporioides PXP-49. In the crystal, mol-ecules are assembled by classical O-H⋯O hydrogen bonds, forming a two-dimensional network, with base vectors [100] and [010]. The absolute configuration was assigned from the measured optical rotation and reference to the literature. An intra-molecular O-H⋯O hydrogen bond occurs.

Treatment of 34 cases of Simple ankle sprain mainly by Ashi point and in cooperation with magnetic therapy, and Qiuxu (GB40), Shenmai(BL62), Jinmen (BL 63) and Pucan (BL 61) were added in the presence of strephenopodia sprain, Zhaohai (KI 6), Shuiquan (KI 5) and Taixi (KI 3) were added in the presence of strephexopodia sprain, the effective rate was 91.7%.