118 research outputs found
High prevalence of Helicobacter pylori infection in Behcetâs disease
Background: Behcetâs disease (BD) is a multisystem disease of unknown etiology. There are several clues which
may indicate an ethiopathogenesis role for Helicobacter pylori infection in this disease.
Methods: In a case control study in an out patient department, 48 patients with BD were compared to age, sex
matched controls regarding presence of H. pylori infection by serology and urea breath test (UBT).
Results: Ongoing H. pylori infection was more prevalent among patients with BD using result of UBT with odds
ratio of 3.1 (95% CI: 1.34 â 7.26, PV < 0.001).
Conclusion: H. pylori infection may have a role in the pathogenesis of BD
Radiosensitivity in breast cancer assessed by the Comet and micronucleus assays
Spontaneous and radiation-induced genetic instability of peripheral blood mononuclear cells derived from unselected breast cancer (BC) patients (n=50) was examined using the single-cell gel electrophoresis (Comet) assay and a modified G2 micronucleus (MN) test. Cells from apparently healthy donors (n=16) and from cancer patients (n=9) with an adverse early skin reaction to radiotherapy (RT) served as references. Nonirradiated cells from the three tested groups exhibited similar baseline levels of DNA fragmentation assessed by the Comet assay. Likewise, the Comet analysis of in vitro irradiated (5âGy) cells did not reveal any significant differences among the three groups with respect to the initial and residual DNA fragmentation, as well as the DNA repair kinetics. The G2 MN test showed that cells from cancer patients with an adverse skin reaction to RT displayed increased frequencies of both spontaneous and radiation-induced MN compared to healthy control or the group of unselected BC patients. Two patients from the latter group developed an increased early skin reaction to RT, which was associated with an increased initial DNA fragmentation in vitro only in one of them. Cells from the other BC patient exhibited a striking slope in the doseâresponse curve detected by the G2 MN test. We also found that previous RT strongly increased both spontaneous and in vitro radiation-induced MN levels, and to a lesser extent, the radiation-induced DNA damage assessed by the Comet assay. These data suggest that clinical radiation may provoke genetic instability and/or induce persistent DNA damage in normal cells of cancer patients, thus leading to increased levels of MN induction and DNA fragmentation after irradiation in vitro. Therefore, care has to be taken when blood samples collected postradiotherapeutically are used to assess the radiosensitivity of cancer patients
The Forward Physics Facility at the High-Luminosity LHC
High energy collisions at the High-Luminosity Large Hadron Collider (LHC) produce a large number of particles along the beam collision axis, outside of the acceptance of existing LHC experiments. The proposed Forward Physics Facility (FPF), to be located several hundred meters from the ATLAS interaction point and shielded by concrete and rock, will host a suite of experiments to probe standard model (SM) processes and search for physics beyond the standard model (BSM). In this report, we review the status of the civil engineering plans and the experiments to explore the diverse physics signals that can be uniquely probed in the forward region. FPF experiments will be sensitive to a broad range of BSM physics through searches for new particle scattering or decay signatures and deviations from SM expectations in high statistics analyses with TeV neutrinos in this low-background environment. High statistics neutrino detection will also provide valuable data for fundamental topics in perturbative and non-perturbative QCD and in weak interactions. Experiments at the FPF will enable synergies between forward particle production at the LHC and astroparticle physics to be exploited. We report here on these physics topics, on infrastructure, detector, and simulation studies, and on future directions to realize the FPF's physics potential
Genome Instability and Bleomicin Sensitivity Test
Procjena individualne osjetljivosti na mutagene Äesto je dio istraĆŸivanja u epidemioloĆĄkim studijama koje prate pojavnost zloÄudnih bolesti u populacijama. Posljedica djelovanja mutagena u genomu izloĆŸenih osoba jest nastanak odreÄene, manje ili veÄe, koliÄine oĆĄteÄenja, uvjetovane individualnim razlikama u osjetljivosti. ViĆĄa razina takve genomske nestabilnosti znaÄi opasnost (rizik) od razvoja zloÄudnih bolesti.
Interindividualne razlike u odgovoru na mutagene obiÄno se povezuju i s promijenjenom (veÄinom smanjenom) sposobnosti (kapacitetom) za popravak DNA. CitogenetiÄke studije su pokazale da je genom tumorskih stanica nestabilniji od normalnih, a time i skloniji akumuliranju oĆĄteÄenja, bilo da je nestabilnost uzrokovana nasljeÄem, izloĆŸenoĆĄÄu ili kombinacijom tih dvaju uÄinaka. U oboljelih ispitanika utvrÄena je poveÄana uÄestalost kromatidnih i kromosomskih aberacija naspram normalne populacije te sklonost
razvoju odreÄenih vrsta neoplazija. U praÄenju povezanosti promijenjenog odgovora i pojavnosti tumora sluĆŸe nam razliÄiti biomarkeri. Kao indirektni pokazatelji uspjeĆĄnosti popravka DNA Äesto se rabe testovi osjetljivosti na mutagene u kulturama limfocita periferne krvi. Jedan od takvih testova je i bleomicinski
test. Radiomimetik i citostatik, a po strukturi glikopeptid, bleomicin se u stanici prevodi u aktivni oblik sposoban cijepati molekulu DNA ĆĄto uzrokuje brojne jednolanÄane i dvolanÄane lomove. Kao jednostavna
i jeftina metoda, zasniva se na utvrÄivanju ukupnog broja jednolanÄanih lomova u kromosomima limfocita uzgajanih u staniÄnoj kulturi koji su u uvjetima in vitro tijekom kasne G2-faze staniÄnog ciklusa bili izloĆŸeni bleomicinu. Ovaj revijalni rad daje pregled utjecaja raznih faktora na rezultate samog testa i pokazuje
njegovu ĆĄiroku primjenu u prouÄavanju genomske nestabilnosti koju najÄeĆĄÄe uzrokuje kombinacija raznih faktora.Estimation of individual susceptibility to mutagens is often a part of epidemiological studies monitoring the appearance of malignant disease in different populations. Genome exposure to mutagens can lead to DNA damage. The rate of damage depends on individual differences in response, which are usually associated with differences in DNA repair capacity. Cytogenetic studies have shown that the genome of tumour cells is less stable than normal cells and therefore accumulates more damage. Tumour patients show a higher
frequency of chromatid and chromosomal aberrations and a predisposition to certain types of tumours.
One of the common biomarkers used in monitoring tumour appearance and changed response to DNA damage is the bleomycin test. In its active form, bleomycin (glycopeptid) is a radiomimetic cytostatic that can damage the DNA molecule and cause multiple single and double strands. The bleomycin test is simple and inexpensive, and is based on scoring chromatid breaks in lymphocytes in vitro exposed to bleomycin during the late G2 phase of the cell cycle. This review looks into different factors that may
affect test results and discusses its wide implementation in studies of genome instability usually caused by a combination of factors
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