H.pylori Infection inhibits Inflammatory Bowel Disease(IBD) by affecting the intestinal flora: A systematic Review

Background: Inflammatory bowel diseases (IBD) are chronic, relapsing-remitting diseases of the gastrointestinal tract, including Crohn’s disease (CD), Ulcerative Colitis (UC), and Unclassified IBD (IBDU). Their pathogenesis involves genes and the environment as cofactors in inducing autoimmunity; mainly, the interactions between enteric pathogens and immunity are studied. For example, Helicobacter pylori (HP) is a common pathogen causing gastric inflammation. However, studies found that the number of people with HP was lower than those with IBD. Therefore, it suggests that HP might protect against IBD. Methods: The search terms "helicobacter pylori," "inflammatory bowel disease," "Crohn's disease," and "ulcerative colitis" were entered into the PubMed database. Embase, Medline, Web of Science, Scopus, PubMed publisher, Cochrane, and Google Scholar were also searched. The HP prevalence rates in IBD patients, CD patients, UC patients, and IBDU patients were calculated. So its to prove that there is an inverse relationship between HP and IBD, each group was compared to a control group. Results: Even when the comparison was made separately between each group of newly diagnosed patients and controls to rule out the possibility of pharmacologic bias, the data showed an inverse relationship between the IBD group and the controls. Conclusion: The results of this review demonstrate a striking inverse association between HP infection and the prevalence of inflammatory bowel disease (IBD), regardless of the type of IBD considered across different geographic regions. Anyway, data should be interpreted with care because more research is needed on this topic that is broader, more prospective, and more consistent. This could lead to new ideas about how the environment could cause IBD. Keywords: Inflammatory bowel disease; Helicobacter pylori; Crohn’s disease; Ulcerative colitis; Colorectal cancer DOI: 10.7176/JMPB/72-04 Publication date: May 31st 202

Расчет распределения примеси и потоков ее миграции у клиновидного двойника на основании макроскопической дислокационной модели

High pressure Raman, IR and X-ray diffraction (XRD) studies have been carried out on C-70(Fe(C5H5)(2))(2) (hereafter, "C-70(Fc)(2)") sheets. Theoretical calculation is further used to analyze the Electron Localization Function (ELF) and charge transfer in the crystal and thus to understand the transformation of C-70(Fc)(2) under pressure. Our results show that even at room temperature dimeric phase and one dimensional (1D) polymer phase of C-70 molecules can be formed at about 3 and 8 GPa, respectively. The polymerization is found to be reversible Upon decompression and the reversibility is related to the pressure-tuned charge transfer, as well as the overridden steric repulsion of counter ions. According to the layered structure of the intercalated ferrocene molecules formed in the crystal, we suggest that ferrocene acts as not only a spacer to restrict the polymerization of C-70 molecules within a layer, but also as charge reservoir to tune the polymerization process. This supplies a possible way for us to design the polymerization of fullerenes at suitable conditions

Apoptosis-inducing effect of 6,7-dimethoxy-4'-hydroxy-8- formylflavon from Nicotiana tabacum L leaf in human hepatoma HepG2 cells via activation of mitochondriamediated apoptotic pathway

Purpose: To study the anti-proliferative and apoptotic influences of 6,7-dimethoxy-4'-hydroxy-8- formylflavon (DHF) from the leaves of Nicotiana tabacum L. in human hepatoma HepG2 cells, and the underlying mechanisms.Methods: The anti-proliferative effect of DHF (10 - 50 μg/mL) on HepG2 cells was assessed by CCK-8 assay. The pro-apoptotic effect of DHF (10, 20 and 30 μg/mL) on HepG2 cells was investigated via flow cytometry, while the mechanisms involved were studied using western blot. Xenograft assay was employed for determination of the in vivo effect of DHF (40 mg/kg/day) on HepG2 cell-induced tumor.Results: The proliferation of HepG2 cells was inhibited by DHF (IC50 = 25.87 μg/mL) due to apoptosis. In addition, xenograft assay revealed that HepG2 cell-induced tumor growth was significantly suppressed by DHF (p < 0.05 or 0.01) without any effects on mice body weights. The expressions of Survivin and Bcl-2 proteins were significantly decreased, while those of Bax, c-caspase-9, and ccaspase- 3 proteins were significantly increased by DHF (p < 0.05 or 0.01), leading to increase in cytoplasmic levels of Smac and cytochrome c proteins.Conclusion: The underlying mechanism DHF-mediated apoptotic changes in HepG2 cells in vitro and in vivo involves induction of the mitochondrial pathway of apoptosis. Thus, DHF is a good drug candidate for the development of an effective therapy for liver cancer.Keywords: 6,7-Dimethoxy-4'-hydroxy-8-formylflavon, HepG2 cells, Hepatoma, Mitochondria, Apoptosis, Bax, Cytochrome C, Survivi

DiVA -Digitala Vetenskapliga Arkivet

IR spectra, TG analysis and x-ray diffraction showed a solvated structure for the as-grown C 60 microtubes. Through a gentle heat-treatment in vacuum, pure C 60 microtubes with single crystalline fcc structure were obtained after the elimination of solvents. It is suggested that the C 60 microtubes form through self-assembly from several individual C 60 nanorods

A Simplified Rice DNA Extraction Protocol for PCR Analysis

Abstract: A simple protocol was established for DNA extraction using etiolated rice seedlings, whereby rice DNA was directly extracted in 0.5 mol/L NaOH solution in a single eppendorf tube. Results of comparative PCR analyses and electrophoresis showed that the DNA extracted using this method was as good and useful as that using standard CTAB method. Key words: DNA extraction; rice; polymerase chain reaction; molecular marker; simple sequence repeats; transgene DNA molecular marker technology has been advancing rapidly during past decades and its application perspective seems very brilliant in crop breeding, varietal purity test of crop seeds and germplasm fingerprinting MATERIALS AND METHODS Materials Seeds of the following conventional and hybrid rice varieties were used in this study: indica hybrid rice Xieyou 92 (Xieqingzao/Hui 92) F 1 and Xieyou 46 (Xieqingzao A/Milyang 46) F 1 , the cytoplasmic male sterile line Xieqingzao A, the DNA extraction DNA was extracted using a modified CTAB method PCR and products analysis PCR amplification of DNA fragments of the cry1Ab gene in transgenic rice and of the microsatellite within the Wx gene in hybrid rice were conducted using the DNA templates isolated by modified CTAB method and our own simplified protocol. The sequences of forward primer and reverse primer for the cry1Ab gene were 5'-TTCCTTGGACGAAATCCCACC-3' and 5'-GCCAGAATTGAACACATGAGCGC-3', targeting a fragment of 559 bp. The forward primer of SSR of Wx gene was 5'-CTTTGTCTATCTCAAGACAC-3' and the reverse primer 5'-TTGCAGATGTTCTTCCTGATG-3', which were designed according to Blight et a

Identification of DHX36 as a tumour suppressor through modulating the activities of the stress-associated proteins and cyclin-dependent kinases in breast cancer

The nucleic acid guanine-quadruplex structures (G4s) are involved in many aspects of cancer progression. The DEAH-box polypeptide 36 (DHX36) has been identified as a dominant nucleic acid helicase which targets and disrupts DNA and RNA G4s in an ATP-dependent manner. However, the actual role of DHX36 in breast cancer remains unknown. In this study, we observed that the gene expression of DHX36 was positively associated with patient survival in breast cancer. The abundance of DHX36 is also linked with pathologic conditions and the stage of breast cancer. By using the xenograft mouse model, we demonstrated that the stable knockdown of DHX36 via lentivirus in breast cancer cells significantly promoted tumour growth. We also found that, after the DHX36 knockdown (KD), the invasion of triple-negative breast cancer cells was enhanced. In addition, we found a significant increase in the number of cells in the S-phase and a reduction of apoptosis with the response to cisplatin. DHX36 KD also desensitized the cytotoxic cellular response to paclitaxel and cisplatin. Transcriptomic profiling analysis by RNA sequencing indicated that DHX36 altered gene expression profile through the upstream activation of TNF, IFNγ, NFκb and TGFβ1. High throughput signalling analysis showed that one cluster of stress-associated kinase proteins including p53, ROCK1 and JNK were suppressed, while the mitotic checkpoint protein-serine kinases CDK1 and CDK2 were activated, as a consequence of the DHX36 knockdown. Our study reveals that DHX36 functions as a tumour suppressor and may be considered as a potential therapeutic target in breast cancer

Identification of DHX36 as a tumour suppressor through modulating the activities of the stress-associated proteins and cyclin-dependent kinases in breast cancer

The nucleic acid guanine-quadruplex structures (G4s) are involved in many aspects of cancer progression. The DEAH-box polypeptide 36 (DHX36) has been identified as a dominant nucleic acid helicase which targets and disrupts DNA and RNA G4s in an ATP-dependent manner. However, the actual role of DHX36 in breast cancer remains unknown. In this study, we observed that the gene expression of DHX36 was positively associated with patient survival in breast cancer. The abundance of DHX36 is also linked with pathologic conditions and the stage of breast cancer. By using the xenograft mouse model, we demonstrated that the stable knockdown of DHX36 via lentivirus in breast cancer cells significantly promoted tumour growth. We also found that, after the DHX36 knockdown (KD), the invasion of triple-negative breast cancer cells was enhanced. In addition, we found a significant increase in the number of cells in the S-phase and a reduction of apoptosis with the response to cisplatin. DHX36 KD also desensitized the cytotoxic cellular response to paclitaxel and cisplatin. Transcriptomic profiling analysis by RNA sequencing indicated that DHX36 altered gene expression profile through the upstream activation of TNF, IFNγ, NFκb and TGFβ1. High throughput signalling analysis showed that one cluster of stress-associated kinase proteins including p53, ROCK1 and JNK were suppressed, while the mitotic checkpoint protein-serine kinases CDK1 and CDK2 were activated, as a consequence of the DHX36 knockdown. Our study reveals that DHX36 functions as a tumour suppressor and may be considered as a potential therapeutic target in breast cancer

Synthesis and biological evaluation of novel bi-gold mitocans in lung cancer cells

Mitochondria are promising drug target for cancer treatment. We previously demonstrated that a bi-gold compound BGC2a was more potent than the mono-gold drug auranofin in suppressing cancer cells due to increased gold atom number that led to higher drug accumulation in and thereby inhibition of mitochondria. To exploit the potential of this new strategy, we further designed and synthesized a series of bi-gold mitocans, the compounds targeting mitochondria. The results showed that most of the newly synthesized mitocans exhibited obviously lower IC50 than auranofin, an old drug that is repurposed in clinical trials for cancer treatment. The best mitocan C3P4 was nearly 2-fold more potent than BGC2a in human non-small cell lung cancer A549 cells and mantle cell lymphoma Jeko-1 cells, exhibiting substantial colony formation-suppressing and tumor-suppressing effects in A549 cells xenograft model. C3P4 induced apoptosis in a dose-dependent manner and arrested cell cycle at G0/G1 phase. The mechanistic study showed that C3P4 significantly increased the global reactive oxygen species and mitochondrial superoxide level, and reduced the mitochondrial membrane potential. C3P4 preferentially accumulated in mitochondria as measured by the gold content and substantially inhibited oxygen consumption rate and ATP production. These results further validated our hypothesis that targeting mitochondria would be promising to develop more potent anticancer agents. C3P4 may be further evaluated as a drug candidate for lung cancer treatment