The Role of Iron Status in the Early Progression of Metronidazole Resistance in Trichomonas vaginalis Under Microaerophilic Conditions

2018 ◽  
Vol 66 (2) ◽  
pp. 309-315 ◽  
Author(s):  
Wendy Argáez-Correa ◽  
María E. Alvarez-Sánchez ◽  
Victor E. Arana-Argáez ◽  
Mario A. Ramírez-Camacho ◽  
Jazmín S. Novelo-Castilla ◽  
...  
Keyword(s):  
Trichomonas Vaginalis ◽  
Iron Status ◽  
Metronidazole Resistance ◽  
Early Progression ◽  
Microaerophilic Conditions

scholarly journals The Role of Endoglin in Hepatocellular Carcinoma

2021 ◽  
Vol 22 (6) ◽  
pp. 3208
Author(s):  
Kuo-Shyang Jeng ◽  
I-Shyan Sheen ◽  
Shu-Sheng Lin ◽  
Chuen-Miin Leu ◽  
Chiung-Fang Chang
Keyword(s):  
Hepatocellular Carcinoma ◽  
Liver Diseases ◽  
Transforming Growth Factor ◽  
Antiangiogenic Therapy ◽  
Transforming Growth Factor Β ◽  
Postoperative Recurrence ◽  
Transmembrane Glycoprotein ◽  
Early Progression

Endoglin (CD105) is a type-1 integral transmembrane glycoprotein and coreceptor for transforming growth factor-β (TGF-β) ligands. The endoglin/TGF-β signaling pathway regulates hemostasis, cell proliferation/migration, extracellular matrix (ECM) synthesis and angiogenesis. Angiogenesis contributes to early progression, invasion, postoperative recurrence, and metastasis in hepatocellular carcinoma (HCC), one of the most widespread malignancies globally. Endoglin is overexpressed in newly formed HCC microvessels. It increases microvessel density in cirrhotic and regenerative HCC nodules. In addition, circulating endoglin is present in HCC patients, suggesting potential for use as a diagnostic or prognostic factor. HCC angiogenesis is dynamic and endoglin expression varies by stage. TRC105 (carotuximab) is an antibody against endoglin, and three of its clinical trials were related to liver diseases. A partial response was achieved when combining TRC105 with sorafenib. Although antiangiogenic therapy still carries some risks, combination therapy with endoglin inhibitors or other targeted therapies holds promise.

scholarly journals Induced Disruption of the Iron-Regulatory Hormone Hepcidin Inhibits Acute Inflammatory Hypoferraemia

2016 ◽  
Vol 8 (5) ◽  
pp. 517-528 ◽  
Author(s):  
Andrew E. Armitage ◽  
Pei Jin Lim ◽  
Joe N. Frost ◽  
Sant-Rayn Pasricha ◽  
Elizabeth J. Soilleux ◽  
...  
Keyword(s):  
Mouse Model ◽  
Transgenic Mouse ◽  
Brucella Abortus ◽  
Serum Iron ◽  
Vibrio Vulnificus ◽  
Iron Status ◽  
Transgenic Mouse Model ◽  
Innate Immune ◽  
Serum Hepcidin

Withdrawal of iron from serum (hypoferraemia) is a conserved innate immune antimicrobial strategy that can withhold this critical nutrient from invading pathogens, impairing their growth. Hepcidin (Hamp1) is the master regulator of iron and its expression is induced by inflammation. Mice lacking Hamp1 from birth rapidly accumulate iron and are susceptible to infection by blood-dwelling siderophilic bacteria such as Vibrio vulnificus. In order to study the innate immune role of hepcidin against a background of normal iron status, we developed a transgenic mouse model of tamoxifen-sensitive conditional Hamp1 deletion (termed iHamp1-KO mice). These mice attain adulthood with an iron status indistinguishable from littermate controls. Hamp1 disruption and the consequent decline of serum hepcidin concentrations occurred within hours of a single tamoxifen dose. We found that the TLR ligands LPS and Pam3CSK4 and heat-killed Brucella abortus caused an equivalent induction of inflammation in control and iHamp1-KO mice. Pam3CSK4 and B. abortus only caused a drop in serum iron in control mice, while hypoferraemia due to LPS was evident but substantially blunted in iHamp1-KO mice. Our results characterise a powerful new model of rapidly inducible hepcidin disruption, and demonstrate the critical contribution of hepcidin to the hypoferraemia of inflammation.

scholarly journals Furazolidone- and Nitrofurantoin-ResistantHelicobacter pylori: Prevalence and Role of Genes Involved in Metronidazole Resistance

2001 ◽  
Vol 45 (1) ◽  
pp. 306-308 ◽  
Author(s):  
Dong H. Kwon ◽  
Miae Lee ◽  
J. J. Kim ◽  
J. G. Kim ◽  
F. A. K. El-Zaatari ◽  
...  
Keyword(s):  
Helicobacter Pylori ◽  
Clinical Isolates ◽  
Metronidazole Resistance ◽  
H Pylori

ABSTRACT The prevalence of furazolidone, nitrofurantoin, and metronidazole resistance among Helicobacter pylori strains was assessed with 431 clinical isolates. Fifty-two percent were metronidazole resistant, compared to 2% (7 of 431) with resistance to furazolidone and nitrofurantoin. All seven furazolidone- and nitrofurantoin-resistant isolates were also metronidazole resistant.rdxA, frxA, and fdxB knockouts did not result in furazolidone or nitrofurantoin resistance. These data suggest that furazolidone and nitrofurantoin may be good alternatives to metronidazole for treating H. pylori infection.

scholarly journals Role of divalent cations, pH, cytoskeleton componentes and surface charge on the adhesion of Trichomonas vaginalis to a polystyrene substrate

1987 ◽  
Vol 82 (3) ◽  
pp. 379-384 ◽  
Author(s):  
Fernando Costa e Silva Filho ◽  
Cezar Antonio Elias ◽  
Wanderley de Souza
Keyword(s):  
Surface Charge ◽  
Incubation Time ◽  
Trichomonas Vaginalis ◽  
Cytochalasin B ◽  
Culture Media ◽  
Divalent Cations ◽  
Polystyrene Beads ◽  
Different Strains ◽  
Adhesion Index

The process of adhesion of three different strains of Trichomonas vaginalis to a polystyrene substrate was analysed. The process of adhesion was dependent on the time of incubation and the pH of the phosphate-buffered solution (PBS) in which the parasites were suspended. The highest indices of adhesion were observed after an incubation time of 60 min at pH 6.6. The adhesion index increased when the parasites were incubated in the presence of culture media or when Ca++ or Mg++ was added to the PBS solution, whereas cytochalasin B, trypsin or neuraminidase reduced adhesion. Incubation of the parasites in the presence of poly-L-lysine facilitated the process of adhesion. Incubation of the parasites or polystyrene beads in the presence of poly-L-lysine led to important changes in their surface charge.

scholarly journals Inflammation in the lungs of patients diagnosed with Cystic Fibrosis: Association with iron deficiency

SURG Journal ◽  
1969 ◽  
Vol 2 (1) ◽  
pp. 3-10
Author(s):  
Dawn Armstrong ◽  
Lindsay Robinson
Keyword(s):  
Cystic Fibrosis ◽  
Iron Deficiency ◽  
Inflammatory Cytokines ◽  
Wide Spectrum ◽  
Iron Status ◽  
Tissue Destruction ◽  
Hypoxic Conditions ◽  
Mediators Of Inflammation ◽  
The Relationship

Cystic Fibrosis (CF) is characterized by a wide spectrum of phenotypic characteristics such as; deep coughing, increased mucous production, and weight loss. However, only recently was the role of inflammation on the etiology of the disease recognized. CF is characterized as a cyclic progression of infective exacerbations and stable periods initiated by the presence of Pseudomonas Aeruginosa (PA). An increase in inflammatory cytokines/mediators and a decrease in anti-inflammatory cytokines contribute to the net inflammation and overall tissue destruction of the lungs. PA is associated with the low iron status that is seen in 60-75% of the CF population, through the presence of iron sequestering siderophores which distract iron from the tissues. Iron deficiency (ID) initiates further symptoms such as; fatigue, tachycardia, weakness, brittle nails etc, in addition to those caused by CF. The colonization of PA may be the cause or a result of increased iron (ferritin) concentrations in the lungs, but independent of the original relationship, results in a decreased iron status. Iron is used by PA under hypoxic conditions such as in the fibrosis lung, as a source of energy. Studies on the relationship between CF and ID contribute a variety of possible causes although currently no direct connection has been discovered. At this stage, further studies in this area are needed. This review will primarily focus on the affects of CF on iron status in humans, and secondarily examine the effect of mediators of inflammation in respects to ID.

scholarly journals The role of genotypes on phosphorus, zinc, manganese and iron status and their relations in leaves of maize on hydromorphic soil

2011 ◽  
Vol 50 (No. 12) ◽  
pp. 535-539 ◽  
Author(s):  
V. Kovačević ◽  
I. Brkić ◽  
D. Šimić ◽  
G. Bukvić ◽  
M. Rastija
Keyword(s):  
Mineral Content ◽  
Zea Mays L ◽  
Iron Status ◽  
Correlation Coefficients ◽  
Hydromorphic Soil ◽  
Maize Hybrids ◽  
Fe Content ◽  
High Repeatability ◽  
Nutritional Imbalance

Hydromorphy is a major soil fertility constraint in Europe and North America causing specific nutritional imbalance in soils and crops. The objectives of this study were to examine the differences among maize hybrids in phosphorus (P), zinc (Zn), manganese (Mn) and iron (Fe) status in leaves, and to investigate the interrelationship among these micronutrients as well as the interrelationship between Zn and P on hydromorphic soil in Eastern Croatia. Twenty maize (Zea mays L.) hybrids were grown under field conditions of Eastern Croatia in a period of two years. Considerable differences in mean ear-leaf Zn, Mn and Fe contents at silking stage were found ranging from 16.3 to 30.0 mg/kg for Zn, from 28.5 to 62.2 mg/kg for Mn and from 137 to 222 mg/kg for Fe content. Mean ratios among nutrients were at acceptable levels: 146 (P:Zn), 7.6 (Fe:Zn) and 3.72 (Fe:Mn). Differences among the hybrids ranged from 95.1 to 210.4 (P:Zn), from 5.3 to 10.4 (Fe:Zn) and from 2.4 to 5.79 (Fe:Mn). Maize hybrids which have higher P:Zn is less acceptable for growing on soils which are either rich in P or moderate in available Zn. Highly significant correlation coefficients between years for mineral content (0.696 for Zn, 0.586 for Mn and 0.525 for Fe) indicated high repeatability estimates within genotypes across the seasons and importance of heredity for nutritional status.

Molecular Epidemiology of Metronidazole Resistance in a Population of Trichomonas vaginalis Clinical Isolates

2000 ◽  
Vol 38 (8) ◽  
pp. 3004-3009 ◽  
Author(s):  
Lauren J. Snipes ◽  
Pascale M. Gamard ◽  
Elizabeth M. Narcisi ◽  
C. Ben Beard ◽  
Tovi Lehmann ◽  
...  
Keyword(s):  
Drug Resistance ◽  
Trichomonas Vaginalis ◽  
Random Amplified Polymorphic Dna ◽  
Transmitted Disease ◽  
Clinical Isolates ◽  
Nucleotide Position ◽  
Sexually Transmitted ◽  
Metronidazole Resistance ◽  
High Level

Trichomonas vaginalis, the causative agent for human trichomoniasis, is a problematic sexually transmitted disease mainly in women, where it may be asymptomatic or cause severe vaginitis and cervicitis. Despite its high prevalence, the genetic variability and drug resistance characteristics of this organism are poorly understood. To address these issues, genetic analyses were performed on 109 clinical isolates using three approaches. First, two internal transcribed spacer (ITS) regions flanking the 5.8S subunit of the ribosomal DNA gene were sequenced. The only variation was a point mutation at nucleotide position 66 of the ITS1 region found in 16 isolates (14.7%). Second, the presence of a 5.5-kb double-stranded RNAT. vaginalis virus (TVV) was assessed. TVV was detected in 55 isolates (50%). Finally, a phylogenetic analysis was performed based on random amplified polymorphic DNA data. The resulting phylogeny indicated at least two distinct lineages that correlate with the presence of TVV. A band-sharing index indicating relatedness was created for different groups of isolates. It demonstrated that isolates harboring the virus are significantly more closely related to each other than to the rest of the population, and it indicated a high level of relatedness among isolates with in vitro metronidazole resistance. This finding is consistent with the hypothesis that drug resistance toT. vaginalis resulted from a single or very few mutational events. Permutation tests and nonparametric analyses showed associations between metronidazole resistance and phylogeny, the ITS mutation, and TVV presence. These results suggest the existence of genetic markers with clinical implications for T. vaginalisinfections.

scholarly journals Role of metronidazole resistance in therapy of Helicobacter pylori infections.

1992 ◽  
Vol 36 (1) ◽  
pp. 163-166 ◽  
Author(s):  
H Rautelin ◽  
K Seppala ◽  
O V Renkonen ◽  
U Vainio ◽  
T U Kosunen
Keyword(s):  
Helicobacter Pylori ◽  
Metronidazole Resistance
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