Objective To discuss on the relationship among innovation,scientific nature and ethics in medical articles,in order to improve the academic quality of manuscripts.Methods Take Chinese Journal of Radiological Medicine and Protection as an example,innovation was emphasized in the field of radiation diagnosis and treatment,while the cases lack of innovation were pointed.However,the lessons from many papers showed that those papers only with innovation would be rejected because of defect in scientific nature and ethics.Results Innovation is the soul of the paper,and the scientific and ethical nature is the foundation and premise of innovation.Conclusions While the innovation is emphasized,the scientific nature and ethics of the thesis should be not ignored.These three aspects are integral.

This study was to improve the way for selecting ura5 mutants of Cryptoccocus neoformans Cap59 capsule-deficient strains.They were induced by Diethyl Sulfate. Ura5 mutants were screened by 5-fluoroorotic acid counter selection method. Using the new method, we obtained two ura5 mutants of Cryptoccocus neoformans Cap59 capsule-deficient strain.A easy method that was used to screen ura5 mutants of Cryptoccocus neoformans has been established.

Writing and publishing scientific papers is a very important part of the research work.The quality of the thesis is also an important indicator to measure the achievements of scientific research workers.The quality of the thesis mainly includes the academic quality and the writing quality,but some of the researchers are mostly proficient in practice and neglect the writing,so there are still many writing problems in the manuscript.By reading the submission specification,this article summarizes the common problems in the writing,so as to provide the reference value for the readers.

BACKGROUND: The study aimed to estimate the value of embryonal natural orifice transluminal endoscopic surgery (ENOTES) in treating severe acute pancreatitis (SAP) complicated with abdominal compartment syndrome (ACS). METHODS: The patients, who were randomized into an ENOTES group and an operative group, underwent ENOTES and laparotomy, respectively. The results and complications of the two groups were compared. RESULTS: Enterocinesia was observed earlier in the ENOTES group than in the operative group. Acute Physiology and Chronic Health Evaluation II (APACHE II) score of patients in the ENOTES group was lower than that of the operative group on the 1st, 3rd and 5th post-operative day (P<0.05). The cure rate was 96.87％ in the ENOTES group, which was statistically different from 78.12％ in the operative group (P<0.05). There were significant differences in complications and mortality between the two groups (P<0.01). CONCLUSION: Compared with surgical decompression, ENOTES associated with flexible endoscope therapy is an effective and minimal invasive procedure with less complications.

To investigate the effects of sorafenib and octreotide combination treatment on cellular proliferation and explore the underlying molecular mechanisms by using an in vitro cell culture system with the human hepatoma cell line, HepG2. HepG2 cells were treated with different concentrations of sorafenib and octreotide alone or in combination. Untreated HepG2 cells were used as controls. Treatment-induced cytotoxicity was determined with the cell counting kit-8 by Sigma-Aldrich, and rate of apoptosis was detected by flow cytometry. Fluorescent microscopy was used to observe rates of cell growth under the various treatments. Treatment-induced changes in protein expressions were detected by enzyme-linked immunosorbent assay (for vascular endothelial growth factor (VEGF)) and Western blotting (for the Mcl-1 apoptosis mediator and the ERK1/2 and PERK1/2 kinases). Sorafenib and octreotide, used alone or in combination, inhibited proliferation and induced apoptosis in HepG2 cells. Combination treatment was more effective than either mono-treatment (F = 200.398, P less than 0.05). Fluorescent microscopy showed that combination treatment stimulated phosphatidylserine, the marker of early apoptosis, better than either mono-treatment. VEGF expression in cultures exposed to combination treatment was also significantly lower than in mono-treatment or untreated control cultures (F = 1019.725, P less than 0.05). Western blotting showed that octreotide mono-treatment had no effect on Mcl-1 expression (vs. control group; P more than 0.05) and that combination treatment significantly lowered Mcl-1 expression (vs. mono-treatment and control groups; P less than 0.05). None of the treatments affected ERK1/2 expression (all, P more than 0.05), while all treatments significantly lowered PERK1/2 expression (vs. control group; F = 2.401, P less than 0.05) and the combination treatment lowered PERK1/2 significantly more than either mono-treatment (P less than 0.05). Sorafenib and octreotide can inhibit proliferation and induce apoptosis in the human hepatoma cell line, HepG2. Combination treatment is significantly more efficacious (P less than 0.05) and produced synergistic effects. The mechanism underlying this phenomenon may depend on synergistic inhibition of VEGF, the anti-apoptotic protein Mcl-1, and the proliferation-inducing PERK1/2.
Apoptosis ; drug effects ; Benzenesulfonates ; pharmacology ; Cell Proliferation ; drug effects ; Hep G2 Cells ; drug effects ; Humans ; Niacinamide ; analogs & derivatives ; Octreotide ; pharmacology ; Phenylurea Compounds ; Pyridines ; pharmacology

OBJECTIVETo study the molecular mechanism of apoptosis of leukemic cells (K562 cells) induced by iron chelating agent deferoxamine (DFO).

METHODSThe exponentially growing K562 cells were used (1×10(6)/mL) in this study. The K562 cells were treated with different concentrations of DFO (10, 50 and 100 mmol/L), DFO+FeCl3 (10 μmol/L each) or normal saline (blank control). The cellular labile iron pool was measured with a fluorimetric assay using the metalsensitive probe calcein-AM. The viable count and cell viability were determined by typanblue assay. Cell apoptosis was determined by morphological study and flow cytometry assay. Caspase-3 activity in K562 cells was detected by colorimetry.

RESULTSAfter DFO treatment, the cellular labile iron pool and the viability of K562 cells were reduced and the cell apoptosis increased in a time- and dose-dependent manner compared with the blank control group. The apoptosis rate of K562 cells in the DFO+FeCl3 treatment group was not significantly different from that in the blank control group. The caspase-3 activity in K562 cells increased significantly 24 hrs after 50 and 100 μmmol DFO treatment when compared with the blank control group (P<0.01). There was a negative correlation between cellular labile iron pool and caspase-3 activity of K562 cells (r=-0.894, P<0.05).

CONCLUSIONSDFO induces apoptosis of leukemic cells possibly through decreasing cellular labile iron pool and increasing caspase-3 activity of the cells.

Apoptosis ; drug effects ; Caspase 3 ; metabolism ; Deferoxamine ; pharmacology ; Flow Cytometry ; Humans ; Iron Chelating Agents ; pharmacology ; K562 Cells

The study aimed to clone the open reading frame of cinnamate 4-hydroxylase (C4H) from Aquilaria sinensis and analyze the bioinformatics and expression of the gene. One unique sequence containing C4H domain was discovered in our previous reported wound transcriptome dataset of A. sinensis. The open reading frame of C4H was cloned by RT-PCR strategy with the template of mixed RNA extracted from A. sinensis stem which treated by different wound time. The bioinformatic analysis of this gene and its corresponding protein was performed. C4H expression profiles in responds to MeJA (methyl jasmonate) application were analyzed by real-time PCR. The length of C4H open reading frame (ORF) was 1 515 bp, encoding 514 amino acids. The GenBank accession number is KF134783. Inducible-experiments showed that the genes were induced by mechanical wound as well as MeJA induction, and reached the highest expression level at 8 h and 20 h, respectively. The full-length cDNA of C4H and its expression patterns will provide a foundation for further research on its function in the molecular mechanisms of aromatic compounds and flavonoids biosynthesis.
Amino Acid Sequence ; Cloning, Molecular ; Models, Molecular ; Molecular Sequence Data ; Open Reading Frames ; Oxidoreductases ; chemistry ; genetics ; metabolism ; Phylogeny ; Plant Proteins ; chemistry ; genetics ; metabolism ; Thymelaeaceae ; chemistry ; enzymology ; genetics ; Trans-Cinnamate 4-Monooxygenase ; chemistry ; genetics ; metabolism

Objective To observe the relationship between apoptosis of K562 cell induced by iron-deprivation and activation of Caspase-3.Methods K562 cells were treated with desferrioxamine(DFO) in different dosages were collected at different time points.K562 cells were labelled with Annexin V/PI,and then the rate of apoptosis was measured by flow cytometry;The activation of Caspase-3 were detected by colorimetric method with pAN labelled substrate;The active protein of Caspase-3 were analyzed by Western blot.Results When K562 cells were treated with different concentrations of DFO,the apoptosis rate and the activity of Caspase-3 increases gradually.When K562 cells were incubated with DFO(50 ?mol/L and 100 ?mol/L) 24 h later,the enzymatic activity of Caspase-3 increases dramatically more than that of control group,and the difference was significantly(P0.05).All those effect above can be counteracted by equal mole concentration of FeCl_3.Conclusion Iron-deprivation maybe induce the apoptosis of K562 cell by chelating intracellular iron and activing Caspase-3.

OBJECTIVETo investigate the effect of Tauroursodeoxycholic acid (TUDCA) on Taurodeoxycholic acid (TDCA)-induced HepG2 cell apoptosis and to clarify the molecular mechanism of its anti-apoptosis effect of TUDCA.

METHODSMorphologic evaluation of apoptotic cells was performed by Hoechst 33258 staining and electron microscope. DNA fragment was detected by electrophoresis on 1.5% agarose gels. Apoptosis rate was measured by flow cytometry using PI dye. Following incubation of HepG2 cells either with TDCA alone, or coincubation with TUDCA and TDCA, the releasing level of cytochrome c from mitochondria into cytosol was determined by western blot, also the activity of caspase-3, 8, 9.

RESULTSIncubating the cells with 400 micromol/L TDCA for 12 h induced the cells apoptosis significantly. The apoptotic rate decreased from 50.35% +/- 2.20% to 13.78% +/- 0.84% after coincubation with TUDCA, and this anti-apoptotic effect of TUDCA was confirmed by morphological and DNA ladder detection. TUDCA significantly inhibited the release of cytochrome C from mitochondria into cytosol, and the activity of caspase-9, 3 (t > or = 13.00, P < 0.01), especially at 12 h, caspase-3 activity decreased by 54.9% (t = 16.88, P < 0.01) and 52.5%, however it had no obvious effect on the activity of caspase-8 (t = 1.94, P > 0.05).

CONCLUSIONSTUDCA prevents HepG2 cells apoptosis induced by TDCA through modulating mitochondrial membrane stability, inhibiting the release of cytochrome c and the activation of procaspase-9 and 3. Anti-apoptotic mechanism of TUDCA may be considered to be one of the most important reasons that TUDCA exerts significant efficacy in the treatment of cholestatic liver diseases.

Apoptosis ; drug effects ; Carcinoma, Hepatocellular ; pathology ; Caspase 3 ; Caspase 9 ; Caspases ; metabolism ; Cytochromes c ; pharmacology ; Humans ; Liver Neoplasms ; pathology ; Taurochenodeoxycholic Acid ; pharmacology ; Taurodeoxycholic Acid ; analogs & derivatives ; pharmacology ; Tumor Cells, Cultured

The inflammatory response is involved in the pathogenesis of the most common types of heart disease.Sanguinarine (SAN) has various pharmacological properties such as anti-inflammatory,antioxidant,antibacterial,antitumor,and immune-enhancing properties.However,few studies have investigated the effects of SAN on lipopolysaccharide (LPS)-induced inflammatory and apoptotic responses in H9c2 cardiomyocytes.Therefore,in this study,H9c2 cells were co-treated with SAN and LPS,and the mRNA levels of pro-inflammation markers and the apoptosis rate were measured to clarify the effect of SAN on cardiac inflammation.The underlying mechanism was further investigated by detecting the activation of Toll-like receptor (TLR)4/nuclear factor-κB (NF-κB) signaling pathways.As a result,increased mRNA expression of interleukin (IL)-1 β,IL-6,and TNFα induced by LPS was attenuated after SAN treatment;LPS-induced apoptosis of H9c2 cardiomyocytes and cleaved-caspase 8,9,3 were all significantly reduced by SAN.Further experiments showed that the beneficial effect of SAN on blocking the inflammation and apoptosis of H9c2 cardiomyocytes induced by LPS was associated with suppression of the TLR4/NF-κB signaling pathway.It was suggested that SAN suppressed the LPS-induced inflammation and apoptosis of H9c2 cardiomyocytes,which may be mediated by inhibition of the TLR4/NF-κB signaling pathway.Thus,SAN may be a feasible therapy to treat sepsis patients with cardiac dysfunction.