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  • AGRIS (United Nations, Food and Agriculture Organization)  (15)
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  • 1
    Language: English
    In: Infection and immunity, June 2011, Vol.79(6), pp.2324-34
    Description: Haemophilus ducreyi resists killing by antimicrobial peptides encountered during human infection, including cathelicidin LL-37, α-defensins, and β-defensins. In this study, we examined the role of the proton motive force-dependent multiple transferable resistance (MTR) transporter in antimicrobial peptide resistance in H. ducreyi. We found a proton motive force-dependent effect on H. ducreyi's resistance to LL-37 and β-defensin HBD-3, but not α-defensin HNP-2. Deletion of the membrane fusion protein MtrC rendered H. ducreyi more sensitive to LL-37 and human β-defensins but had relatively little effect on α-defensin resistance. The mtrC mutant 35000HPmtrC exhibited phenotypic changes in outer membrane protein profiles, colony morphology, and serum sensitivity, which were restored to wild type by trans-complementation with mtrC. Similar phenotypes were reported in a cpxA mutant; activation of the two-component CpxRA regulator was confirmed by showing transcriptional effects on CpxRA-regulated genes in 35000HPmtrC. A cpxR mutant had wild-type levels of antimicrobial peptide resistance; a cpxA mutation had little effect on defensin resistance but led to increased sensitivity to LL-37. 35000HPmtrC was more sensitive than the cpxA mutant to LL-37, indicating that MTR contributed to LL-37 resistance independent of the CpxRA regulon. The CpxRA regulon did not affect proton motive force-dependent antimicrobial peptide resistance; however, 35000HPmtrC had lost proton motive force-dependent peptide resistance, suggesting that the MTR transporter promotes proton motive force-dependent resistance to LL-37 and human β-defensins. This is the first report of a β-defensin resistance mechanism in H. ducreyi and shows that LL-37 resistance in H. ducreyi is multifactorial.
    Keywords: Antimicrobial Cationic Peptides -- Metabolism ; Bacterial Outer Membrane Proteins -- Immunology ; Chancroid -- Microbiology ; Haemophilus Ducreyi -- Pathogenicity ; Regulon -- Genetics
    ISSN: 00199567
    E-ISSN: 1098-5522
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  • 2
    In: Infection and Immunity, 2010, Vol. 78(3), p.1176
    Description: Haemophilus ducreyi is an extracellular pathogen of human epithelial surfaces that resists human antimicrobial peptides (APs). The organism's genome contains homologs of genes sensitive to antimicrobial peptides (sap operon) in nontypeable Haemophilus influenzae. In this study, we characterized the sap-containing loci of H. ducreyi 35000HP and demonstrated that sapA is expressed in broth cultures and H. ducreyi-infected tissue; sapA is also conserved among both class I and class II H. ducreyi strains. We constructed a nonpolar sapA mutant of H. ducreyi 35000HP, designated 35000HPsapA, and compared the percent survival of wild-type 35000HP and 35000HPsapA exposed to several human APs, including alpha-defensins, beta-defensins, and the cathelicidin LL-37. Unlike an H. influenzae sapA mutant, strain 35000HPsapA was not more susceptible to defensins than strain 35000HP was. However, we observed a significant decrease in the survival of strain 35000HPsapA after exposure to LL-37, which was complemented by introducing sapA in trans. Thus, the Sap transporter plays a role in resistance of H. ducreyi to LL-37. We next compared mutant strain 35000HPsapA with strain 35000HP for their ability to cause disease in human volunteers. Although both strains caused papules to form at similar rates, the pustule formation rate at sites inoculated with 35000HPsapA was significantly lower than that of sites inoculated with 35000HP (33.3% versus 66.7%; P = 0.007). Together, these data establish that SapA acts as a virulence factor and as one mechanism for H. ducreyi to resist killing by antimicrobial peptides. To our knowledge, this is the first demonstration that an antimicrobial peptide resistance mechanism contributes to bacterial virulence in humans.
    Keywords: Medicine ; Biology;
    ISSN: 0019-9567
    ISSN: 00199567
    E-ISSN: 10985522
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  • 3
    Language: English
    In: Veterinary Microbiology, 2008, Vol.131(3), pp.215-228
    Description: As laying hens age, egg production and quality decreases. Egg producers can impose an induced molt on older hens that results in increased egg productivity and decreased hen mortality compared with non-molted hens of the same age. This review discusses the effect of induced molting by feed removal on immune parameters, serovar Enteritidis (SE) invasion and subsequent production of SE-contaminated eggs. Experimental oral infections with SE show molted hens are more susceptible to SE infection and produce more SE-contaminated eggs in the first few weeks post-molt compared with pre-molt egg production. In addition, it appears that molted hens are more likely to disseminate SE into their environment. Molted hens are more susceptible to SE infection by contact exposure to experimentally infected hens; thus, transmission of SE among molted hens could be more rapid than non-molted birds. Histological examination of the gastrointestinal tracts of molted SE-infected hens revealed more frequent and severe intestinal mucosal lesions compared with non-molted SE-infected hens. These data suggest that induced molting by feed deprivation alters the normal asymptomatic host–pathogen relationship. Published data suggest the highest proportion of SE-positive eggs is produced within 1–5 weeks post-molt and decreases sharply by 6–10 weeks and dissipates to the background level for non-molted hens by 11–20 weeks. Appropriate treatment measures of eggs produced in the fist 5 weeks post-molting may decrease the risk of foodborne infections to humans.
    Keywords: Molting ; Salmonella ; Enteritidis ; Feed Removal ; Biology ; Veterinary Medicine
    ISSN: 0378-1135
    E-ISSN: 1873-2542
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  • 4
    Language: English
    In: The Lancet, 26 January 2013, Vol.381(9863), pp.295-302
    Description: Until now, only imatinib and sunitinib have proven clinical benefit in patients with gastrointestinal stromal tumours (GIST), but almost all metastatic GIST eventually develop resistance to these agents, resulting in fatal disease progression. We aimed to assess efficacy and safety of regorafenib in patients with metastatic or unresectable GIST progressing after failure of at least imatinib and sunitinib. We did this phase 3 trial at 57 hospitals in 17 countries. Patients with histologically confirmed, metastatic or unresectable GIST, with failure of at least previous imatinib and sunitinib were randomised in a 2:1 ratio (by computer-generated randomisation list and interactive voice response system; preallocated block design (block size 12); stratified by treatment line and geographical region) to receive either oral regorafenib 160 mg daily or placebo, plus best supportive care in both groups, for the first 3 weeks of each 4 week cycle. The study sponsor, participants, and investigators were masked to treatment assignment. The primary endpoint was progression-free survival (PFS). At disease progression, patients assigned placebo could crossover to open-label regorafenib. Analyses were by intention to treat. This trial is registered with , number . From Jan 4, to Aug 18, 2011, 240 patients were screened and 199 were randomised to receive regorafenib (n=133) or matching placebo (n=66). Data cutoff was Jan 26, 2012. Median PFS per independent blinded central review was 4·8 months (IQR 1·4–9·2) for regorafenib and 0·9 months (0·9–1·8) for placebo (hazard ratio [HR] 0·27, 95% CI 0·19–0·39; p〈0·0001). After progression, 56 patients (85%) assigned placebo crossed over to regorafenib. Drug-related adverse events were reported in 130 (98%) patients assigned regorafenib and 45 (68%) patients assigned placebo. The most common regorafenib-related adverse events of grade 3 or higher were hypertension (31 of 132, 23%), hand-foot skin reaction (26 of 132, 20%), and diarrhoea (seven of 132, 5%). The results of this study show that oral regorafenib can provide a significant improvement in progression-free survival compared with placebo in patients with metastatic GIST after progression on standard treatments. As far as we are aware, this is the first clinical trial to show benefit from a kinase inhibitor in this highly refractory population of patients. Bayer HealthCare Pharmaceuticals.
    Keywords: Medicine
    ISSN: 0140-6736
    E-ISSN: 1474-547X
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  • 5
    Language: English
    In: PLoS ONE, 2009, Vol.4(5), p.e5578
    Description: Avicins, a class of electrophilic triterpenoids with pro-apoptotic, anti-inflammatory and antioxidant properties, have been shown to induce redox-dependant post-translational modification of cysteine residues to regulate protein function. Based on (a) the cross-talk that occurs between redox and phosphorylation processes, and (b) the role of Stat3 in the process of apoptosis and carcinogenesis, we chose to study the effects of avicins on the processes of phosphorylation/dephosphorylation in Stat3. Avicins dephosphorylate Stat3 in a variety of human tumor cell lines, leading to a decrease in the transcriptional activity of Stat3. The expression of Stat3-regulated proteins such as c-myc, cyclin D1, Bcl2, survivin and VEGF were reduced in response to avicin treatment. Underlying avicin-induced dephosphorylation of Stat3 was dephosphorylation of JAKs, as well as activation of protein phosphatase-1. Downregulation of both Stat3 activity and expression of Stat 3-controlled pro-survival proteins, contributes to the induction of apoptosis in avicin treated tumor cells. Based on the role of Stat3 in inflammation and wounding, and the in vivo inhibition of VEGF by avicins in a mouse skin carcinogenesis model, it is likely that avicin-induced inhibition of Stat3 activity results in the suppression of the pro-inflammatory and pro-oxidant stromal environment of tumors. Activation of PP-1, which also acts as a cellular economizer, combined with the redox regulation by avicins, can aid in redirecting metabolism from growth promoting anabolic to energy sparing pathways.
    Keywords: Research Article ; Cell Biology ; Oncology ; Cell Biology -- Cell Signaling
    E-ISSN: 1932-6203
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  • 6
    Language: English
    In: Plant Physiology, 1 October 1983, Vol.73(2), pp.286-290
    Description: The number of nodules which develop on the primary root of soybean seedlings (Glycine max L. Merr) after inoculation with Rhizobium japonicum is substantially diminished in the region of the root developmentally 10 to 15 hours younger than the region maximally susceptible to nodulation at the time of inoculation. This rapid inhibition of nodulation has been investigated by inoculating soybean seedlings with rhizobia at two different times, 15 hours apart. Living R. japonicum cells, but not heterologous rhizobia or UV-killed cells of the homologous bacterium, were capable of eliciting the rapid inhibitory response. Nodulation responses to varying inoculum concentrations showed that bacterial dosages could be superoptimal, resulting in reduced nodulation and reduced inhibition of nodulation. When suspensions of R. japonicum were dripped uniformly onto the root surfaces, the degree of inhibition of nodulation in developmentally younger regions of the root was correlated with the number of nodules formed in the older and initially most susceptible region of the root. Nodulation in the developmentally younger region of the root, however, was affected very little if the first inoculum was restricted to contact with root cells in the region initially most susceptible to nodulation. The rapid regulatory response may be an important factor contributing to the clustering of nodules in the crown region of soybean roots in field-grown plants and the sparse nodulation commonly observed in younger regions of the root.
    Keywords: Biological sciences -- Biology -- Botany ; Health sciences -- Medical sciences -- Immunology ; Biological sciences -- Biology -- Botany ; Biological sciences -- Biology -- Developmental biology ; Biological sciences -- Biology -- Microbiology ; Health sciences -- Medical conditions -- Diseases ; Biological sciences -- Biology -- Botany ; Applied sciences -- Food science -- Foodstuffs ; Health sciences -- Medical conditions -- Infections ; Biological sciences -- Biology -- Microbiology
    ISSN: 00320889
    E-ISSN: 15322548
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  • 7
    Language: English
    In: PLoS ONE, 2009, Vol.4(12), p.e8115
    Description: There has been much interest in targeting intracellular redox pathways as a therapeutic approach for cancer. Given recent data to suggest that the redox status of extracellular protein thiol groups (i.e. exofacial thiols) effects cell behavior, we hypothesized that redox active anti-cancer agents would modulate exofacial protein thiols. ; To test this hypothesis, we used the sesquiterpene lactone parthenolide, a known anti-cancer agent. Using flow cytometry, and western blotting to label free thiols with Alexa Fluor 633 C maleimide dye and N-(biotinoyl)-N-(iodoacetyl) ethylendiamine (BIAM), respectively, we show that parthenolide decreases the level of free exofacial thiols on Granta mantle lymphoma cells. In addition, we used immuno-precipitation techniques to identify the central redox regulator thioredoxin, as one of the surface protein thiol targets modified by parthenolide. To examine the functional role of parthenolide induced surface protein thiol modification, we pretreated Granta cells with cell impermeable glutathione (GSH), prior to exposure to parthenolide, and showed that GSH pretreatment; (a) inhibited the interaction of parthenolide with exofacial thiols; (b) inhibited parthenolide mediated activation of JNK and inhibition of NFκB, two well established mechanisms of parthenolide activity and; (c) blocked the cytotoxic activity of parthenolide. That GSH had no effect on the parthenolide induced generation of intracellular reactive oxygen species supports the fact that GSH had no effect on intracellular redox. Together these data support the likelihood that GSH inhibits the effect of parthenolide on JNK, NFκB and cell death through its direct inhibition of parthenolide's modulation of exofacial thiols. ; Based on these data, we postulate that one component of parthenolide's anti-lymphoma activity derives from its ability to modify the redox state of critical exofacial thiols. Further, we propose that cancer cell exofacial thiols may be important and novel targets for therapy.
    Keywords: Research Article ; Biochemistry ; Hematology ; Hematology -- Acute Lymphoblastic Leukemia ; Hematology -- Acute Myeloid Leukemia ; Oncology -- Myelomas And Lymphoproliferative Diseases ; Oncology -- Myeloproliferative Disorders, Including Chronic Myeloid Leukemia
    E-ISSN: 1932-6203
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  • 8
    Language: English
    In: Cancer Causes & Control, 2010, Vol.21(3), pp.387-391
    Description: To determine the relationship between 25(OH) vitamin D levels and non-melanoma skin cancer (NMSC), we performed a nested case–control study in ambulatory, elderly men enrolled in the Osteoporotic Fractures in Men (MrOS) Study. Health habit and medical history, including self-reported history of NMSC were recorded and 25(OH)D levels were measured on serum collected at baseline from a random sample of Caucasian MrOS subjects. Mean age (73 ± 5), BMI, daily vitamin D and calcium intake were similar in the men with ( n  = 178) and without NMSC ( n  = 930), but higher levels of 25(OH)D were associated with a decreased risk of having a history of NMSC ( P trend  = 0.04). Men in the highest quintile of 25(OH)D (〉30 ng/mL) had 47% lower odds of NMSC (95% CI: 0.30–0.93, p  = 0.026) compared to those in the lowest quintile. Our results suggest that a diagnosis of NMSC is not a surrogate for adequate 25(OH)D levels or increased UV exposure, and high 25(OH)D levels may be associated with a reduced risk of NMSC.
    Keywords: Skin cancer ; Vitamin D ; Prevention
    ISSN: 0957-5243
    E-ISSN: 1573-7225
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  • 9
    Language: English
    In: In Vitro Cellular & Developmental Biology - Animal, 2010, Vol.46(9), pp.727-732
    Description: Cell misidentification and cross-contamination have plagued biomedical research for as long as cells have been employed as research tools. Examples of misidentified cell lines continue to surface to this day. Efforts to eradicate the problem by raising awareness of the issue and by asking scientists voluntarily to take appropriate actions have not been successful. Unambiguous cell authentication is an essential step in the scientific process and should be an inherent consideration during peer review of papers submitted for publication or during review of grants submitted for funding. In order to facilitate proper identity testing, accurate, reliable, inexpensive, and standardized methods for authentication of cells and cell lines must be made available. To this end, an international team of scientists is, at this time, preparing a consensus standard on the authentication of human cells using short tandem repeat (STR) profiling. This standard, which will be submitted for review and approval as an American National Standard by the American National Standards Institute, will provide investigators guidance on the use of STR profiling for authenticating human cell lines. Such guidance will include methodological detail on the preparation of the DNA sample, the appropriate numbers and types of loci to be evaluated, and the interpretation and quality control of the results. Associated with the standard itself will be the establishment and maintenance of a public STR profile database under the auspices of the National Center for Biotechnology Information. The consensus standard is anticipated to be adopted by granting agencies and scientific journals as appropriate methodology for authenticating human cell lines, stem cells, and tissues.
    Keywords: Cell authentication ; STR profiling ; Consensus standard ; Quality control
    ISSN: 1071-2690
    E-ISSN: 1543-706X
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  • 10
    Language: English
    In: Journal of food protection, March 2008, Vol.71(3), pp.539-44
    Description: The effect of direct-fed microbials (DFM) on fecal shedding of Escherichia coli O157:H7 and Salmonella in naturally infected feedlot cattle was evaluated in a clinical trial involving 138 feedlot steers. Following standard laboratory methods, fecal samples collected from steers were evaluated for change in the detectable levels of E. coli O157:H7 and Salmonella shed in feces after DFM treatment. Sampling of steers was carried out every 3 weeks for 84 days. A significant reduction (32%) in fecal shedding of E. coli O157:H7 (P 〈 0.001), but not Salmonella (P = 0.24), was observed among the treatment steers compared with the control group during finishing. The probability of recovery of E. coli O157:H7 from the feces of treated and control steers was 34.0 and 66.0%, respectively. Steers placed on DFM supplement were almost three times less likely to shed E. coli O157:H7 (odds ratio, 0.36; 95% confidence interval, 0.25 to 0.53; P 〈 0.001) in their feces as opposed to their control counterparts. The probability of recovery of Salmonella from the feces of the control (14.0%) and the treated (11.3%) steers was similar. However, the DFM significantly reduced probability of new infections with Salmonella among DFM-treated cattle compared with controls (nontreated ones). It appears that DFM as applied in our study are capable of significantly reducing fecal shedding of E. coli O157:H7 in naturally infected cattle but not Salmonella. The factors responsible for the observed difference in the effects of DFM on E. coli O157:H7 and Salmonella warrants further investigation.
    Keywords: Probiotics ; Escherichia Coli O157 -- Growth & Development ; Feces -- Microbiology ; Food Contamination -- Prevention & Control ; Lactobacillus Acidophilus -- Physiology ; Propionibacterium -- Physiology ; Salmonella -- Growth & Development
    ISSN: 0362-028X
    E-ISSN: 19449097
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