Journal articles on the topic 'Growth plate Diseases'
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Xie, Yangli, Siru Zhou, Hangang Chen, Xiaolan Du, and Lin Chen. "RECENT RESEARCH ON THE GROWTH PLATE: Advances in fibroblast growth factor signaling in growth plate development and disorders." Journal of Molecular Endocrinology 53, no. 1 (August 2014): T11—T34. http://dx.doi.org/10.1530/jme-14-0012.
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Skeletons are formed through two distinct developmental actions, intramembranous ossification and endochondral ossification. During embryonic development, most bone is formed by endochondral ossification. The growth plate is the developmental center for endochondral ossification. Multiple signaling pathways participate in the regulation of endochondral ossification. Fibroblast growth factor (FGF)/FGF receptor (FGFR) signaling has been found to play a vital role in the development and maintenance of growth plates. Missense mutations inFGFsandFGFRscan cause multiple genetic skeletal diseases with disordered endochondral ossification. Clarifying the molecular mechanisms of FGFs/FGFRs signaling in skeletal development and genetic skeletal diseases will have implications for the development of therapies for FGF-signaling-related skeletal dysplasias and growth plate injuries. In this review, we summarize the recent advances in elucidating the role of FGFs/FGFRs signaling in growth plate development, genetic skeletal disorders, and the promising therapies for those genetic skeletal diseases resulting from FGFs/FGFRs dysfunction. Finally, we also examine the potential important research in this field in the future.
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Holzer, Tatjana, Kristina Probst, Julia Etich, Markus Auler, Veronika S. Georgieva, Björn Bluhm, Christian Frie, et al. "Respiratory chain inactivation links cartilage-mediated growth retardation to mitochondrial diseases." Journal of Cell Biology 218, no. 6 (May 13, 2019): 1853–70. http://dx.doi.org/10.1083/jcb.201809056.
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In childhood, skeletal growth is driven by transient expansion of cartilage in the growth plate. The common belief is that energy production in this hypoxic tissue mainly relies on anaerobic glycolysis and not on mitochondrial respiratory chain (RC) activity. However, children with mitochondrial diseases causing RC dysfunction often present with short stature, which indicates that RC activity may be essential for cartilage-mediated skeletal growth. To elucidate the role of the mitochondrial RC in cartilage growth and pathology, we generated mice with impaired RC function in cartilage. These mice develop normally until birth, but their later growth is retarded. A detailed molecular analysis revealed that metabolic signaling and extracellular matrix formation is disturbed and induces cell death at the cartilage–bone junction to cause a chondrodysplasia-like phenotype. Hence, the results demonstrate the overall importance of the metabolic switch from fetal glycolysis to postnatal RC activation in growth plate cartilage and explain why RC dysfunction can cause short stature in children with mitochondrial diseases.
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Gersing, Alexandra S., Klaus Woertler, Pia M. Jungmann, Christine Bollwein, and Benedikt J. Schwaiger. "Vertebrae, Vertebral End Plates, and Disks: Concepts and Specific Pathologies." Seminars in Musculoskeletal Radiology 23, no. 05 (September 25, 2019): 489–96. http://dx.doi.org/10.1055/s-0039-1693976.
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AbstractVertebral end plates cover the osseous vertebral body. The integrity of the cartilaginous end plates is of great importance for the entire vertebral segment because the vascularized end plate provides the nutrition for the avascular disk. Yet several pathologies may occur at these end plates at the embryonic stage, in childhood to adolescence (e.g., ossification and segmentation disorders of the spine, persistent notochord, slippage of the growth plate), as well as in the mature spine of an adult (degenerative disk disease), that may impact the integrity of the cartilaginous end plate and therefore lead to severe diseases of the spine. This article reviews specific congenital, developmental, and degenerative disorders of the vertebral end plate as well as both established and newly introduced imaging techniques, such as ultrashort echo time imaging based on magnetic resonance imaging, that are suitable for imaging of the end plate.
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Sederquist, Bettina, Paola Fernandez-Vojvodich, Farasat Zaman, and Lars Sävendahl. "RECENT RESEARCH ON THE GROWTH PLATE: Impact of inflammatory cytokines on longitudinal bone growth." Journal of Molecular Endocrinology 53, no. 1 (April 7, 2014): T35—T44. http://dx.doi.org/10.1530/jme-14-0006.
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Children with inflammatory diseases usually display abnormal growth patterns as well as delayed puberty. This is a result of several factors related to the disease itself, such as malnutrition, hypercortisolism, and elevated levels of pro-inflammatory cytokines. These factors in combination with glucocorticoid treatment contribute to growth retardation during chronic inflammation by systemically affecting the major regulator of growth, the GH/IGF1 axis. However, recent studies have also shown evidence of a direct effect of these factors at the growth plate level. In conditions of chronic inflammation, pro-inflammatory cytokines are upregulated and released into the circulation. The most abundant of these, tumor necrosis factor α, interleukin 1β (IL1β), and IL6, are all known to directly act on growth plate cartilage to induce apoptosis and thereby suppress bone growth. Both clinical and experimental studies have shown that growth retardation can partly be rescued when these cytokines are blocked. Therefore, therapy modulating the local actions of these cytokines may be effective for preventing growth failure in patients with chronic inflammatory disorders. In this review, we report the current knowledge of inflammatory cytokines and their role in regulating bone growth.
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Guevara-Morales, Johana M., Michael Frohbergh, Hector Castro-Abril, Juan J. Vaca-González, Luis A. Barrera, Diego A. Garzón-Alvarado, Edward Schuchman, and Calogera Simonaro. "Growth Plate Pathology in the Mucopolysaccharidosis Type VI Rat Model—An Experimental and Computational Approach." Diagnostics 10, no. 6 (May 31, 2020): 360. http://dx.doi.org/10.3390/diagnostics10060360.
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Background: Mucopolysaccharidoses (MPS) are a group of inherited metabolic diseases caused by impaired function or absence of lysosomal enzymes involved in degradation of glycosaminoglycans. Clinically, MPS are skeletal dysplasias, characterized by cartilage abnormalities and disturbances in the process of endochondral ossification. Histologic abnormalities of growth cartilage have been reported at advanced stages of the disease, but information regarding growth plate pathology progression either in humans or in animal models, as well as its pathophysiology, is limited. Methods: Histological analyses of distal femur growth plates of wild type (WT) and mucopolysaccharidosis type VI (MPS VI) rats at different stages of development were performed, including quantitative data. Experimental findings were then analyzed in a theoretical scenario. Results: Histological evaluation showed a progressive loss of histological architecture within the growth plate. Furthermore, in silico simulation suggest the abnormal cell distribution in the tissue may lead to alterations in biochemical gradients, which may be one of the factors contributing to the growth plate abnormalities observed, highlighting aspects that must be the focus of future experimental works. Conclusion: The results presented shed some light on the progression of growth plate alterations observed in MPS VI and evidence the potentiality of combined theoretical and experimental approaches to better understand pathological scenarios, which is a necessary step to improve the search for novel therapeutic approaches.
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Kosowska-Shick, Klaudia, Lois M. Ednie, Pamela McGhee, Kathy Smith, Cynthia D. Todd, Amanda Wehler, and Peter C. Appelbaum. "Incidence and Characteristics of Vancomycin Nonsusceptible Strains of Methicillin-Resistant Staphylococcus aureus at Hershey Medical Center." Antimicrobial Agents and Chemotherapy 52, no. 12 (October 6, 2008): 4510–13. http://dx.doi.org/10.1128/aac.01073-08.
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ABSTRACT All 982 methicillin-resistant Staphylococcus aureus strains collected from August 2006 to December 2007 were tested for vancomycin susceptibility by using 3-μg/ml vancomycin brain heart infusion screening plates, a vancomycin Etest, and a vancomycin/teicoplanin macro Etest. Three vancomycin-intermediate Staphylococcus aureus (VISA) (0.3%) and two heterogeneous VISA (0.2%) isolates were identified. The screening method yielded 895 cases of ≤1 colony and 87 positive results (with growth of >1 colony after 48 h); further Etests showed 82/87 isolates with growth on screening plates to be false positive. Repeat testing showed a false-positivity rate of only 15 of the original 87 isolates by plate screening.
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Evans, K. D., L. E. Sheppard, D. I. Grossman, S. H. Rao, R. B. Martin, and A. M. Oberbauer. "Long Term Cyclic Pamidronate Reduces Bone Growth by Inhibiting Osteoclast Mediated Cartilage-to-Bone Turnover in the Mouse." Open Orthopaedics Journal 2, no. 1 (July 14, 2008): 121–25. http://dx.doi.org/10.2174/1874325000802010121.
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Bisphosphonates, used to treat diseases exhibiting increased osteoclast activity, reduce longitudinal bone growth through an as yet undefined mechanism. Pamidronate, an aminobisphosphonate, was given weekly to mice at 0, 1.25, or 2.50 mg/kg/wk beginning at 4 weeks of age. At 12 weeks of age, humeral length, growth plate area, regional chondrocyte cell numbers, chondrocyte apoptosis, TRAP stained osteoclast number, and osteoclast function assessed by cathepsin K immunohistochemistry were quantified. Humeral length was decreased in pamidronate treated mice compared to vehicle control mice, and correlated with greater growth plate areas reflecting greater proliferative and hypertrophic chondrocyte cell numbers with fewer hypertrophic cells undergoing apoptosis. Pamidronate treatment increased TRAP stained osteoclast numbers yet decreased cathepsin K indicating that pamidronate repressed osteoclast maturation and function. The data suggest that long term cyclic pamidronate treatment impairs bone growth by inhibition of osteoclast maturation thereby reducing cartilage-to-bone turnover within the growth plate.
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Jeremic, Svetlana, Vladimir Radosavljevic, and Dobrila Jakic-Dimic. "Current bacterial diseases of fresh water fishes." Biotehnologija u stocarstvu 21, no. 3-4 (2005): 141–51. http://dx.doi.org/10.2298/bah0504141j.
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From the beginning of fish cultivation, diseases have appeared as a serious problem in this branch of agriculture. In recent years, by the intensifying of production, fish diseases have become even more significant and complex field. Bacterial diseases are constant threat for fish farming, and because of rapid course and severity of clinical manifestations the represent significant part of fish pathology, and also have great economical importance. Harmful effects of bacterial diseases on fishes are: increased morbidity and mortality rate, decreased feed conversion efficiency, decreased growth rates, weakening of fishes, and reproduction problems. In order to examine epizootiological situation and occurrence of bacterial diseases among cultured fish in Serbia, three year research was carried out in 7 carp farms and 3 rainbow trout farms. Also, regular systematic examinations were conducted. Samples of internal organs, skin and gills were inoculated with streak-plate technique on standard and differential culture media plates. Inoculated plates were incubated for 24-48 hours at 20?C and 30?C. After incubation period, colonies were examined, and determination was done on the basis of following characteristics of colonies: form, color, mucosity granulation, roughness and hemolytic properties. Determination of bacterial isolates was done by using API 20E, API rapid. API Coryne systems, and by agglutination method with hyper immune aera. The most frequent diseases among the farmed carp and rainbow trout populations in the examined fish farms were: Bacterial gill disease, Columnaris disease. Yersiniosis Renibacteriosis, Erythrodermatitis. Motile Aeromonas and Pseudomonas infections. Based on the obtained results, modern diagnostic methods were implemented and proper prevention and successful therapy was taken.
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Martsyniak, S. M., and S. S. Strafun. "Surgical treatment of multidimensional deformities of lower limbs before closure of the growth plate in children with rachitic diseases." TRAUMA 21, no. 2 (March 1, 2020): 17–23. http://dx.doi.org/10.22141/1608-1706.2.21.2020.202229.
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Haseeb, Abdul, Ranjan Kc, Marco Angelozzi, Charles de Charleroy, Danielle Rux, Robert J. Tower, Lutian Yao, et al. "SOX9 keeps growth plates and articular cartilage healthy by inhibiting chondrocyte dedifferentiation/osteoblastic redifferentiation." Proceedings of the National Academy of Sciences 118, no. 8 (February 17, 2021): e2019152118. http://dx.doi.org/10.1073/pnas.2019152118.
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Cartilage is essential throughout vertebrate life. It starts developing in embryos when osteochondroprogenitor cells commit to chondrogenesis, activate a pancartilaginous program to form cartilaginous skeletal primordia, and also embrace a growth-plate program to drive skeletal growth or an articular program to build permanent joint cartilage. Various forms of cartilage malformation and degeneration diseases afflict humans, but underlying mechanisms are still incompletely understood and treatment options suboptimal. The transcription factor SOX9 is required for embryonic chondrogenesis, but its postnatal roles remain unclear, despite evidence that it is down-regulated in osteoarthritis and heterozygously inactivated in campomelic dysplasia, a severe skeletal dysplasia characterized postnatally by small stature and kyphoscoliosis. Using conditional knockout mice and high-throughput sequencing assays, we show here that SOX9 is required postnatally to prevent growth-plate closure and preosteoarthritic deterioration of articular cartilage. Its deficiency prompts growth-plate chondrocytes at all stages to swiftly reach a terminal/dedifferentiated stage marked by expression of chondrocyte-specific (Mgp) and progenitor-specific (Nt5e and Sox4) genes. Up-regulation of osteogenic genes (Runx2, Sp7, and Postn) and overt osteoblastogenesis quickly ensue. SOX9 deficiency does not perturb the articular program, except in load-bearing regions, where it also provokes chondrocyte-to-osteoblast conversion via a progenitor stage. Pathway analyses support roles for SOX9 in controlling TGFβ and BMP signaling activities during this cell lineage transition. Altogether, these findings deepen our current understanding of the cellular and molecular mechanisms that specifically ensure lifelong growth-plate and articular cartilage vigor by identifying osteogenic plasticity of growth-plate and articular chondrocytes and a SOX9-countered chondrocyte dedifferentiation/osteoblast redifferentiation process.
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Costantini, Alice, Mari H. Muurinen, and Outi Mäkitie. "New gene discoveries in skeletal diseases with short stature." Endocrine Connections 10, no. 5 (May 1, 2021): R160—R174. http://dx.doi.org/10.1530/ec-21-0083.
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In the last decade, the widespread use of massively parallel sequencing has considerably boosted the number of novel gene discoveries in monogenic skeletal diseases with short stature. Defects in genes playing a role in the maintenance and function of the growth plate, the site of longitudinal bone growth, are a well-known cause of skeletal diseases with short stature. However, several genes involved in extracellular matrix composition or maintenance as well as genes partaking in various biological processes have also been characterized. This review aims to describe the latest genetic findings in spondyloepiphyseal dysplasias, spondyloepimetaphyseal dysplasias, and some monogenic forms of isolated short stature. Some examples of novel genetic mechanisms leading to skeletal conditions with short stature will be described. Strategies on how to successfully characterize novel skeletal phenotypes with short stature and genetic approaches to detect and validate novel gene-disease correlations will be discussed in detail. In summary, we review the latest gene discoveries underlying skeletal diseases with short stature and emphasize the importance of characterizing novel molecular mechanisms for genetic counseling, for an optimal management of the disease, and for therapeutic innovations.
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Gubbels, Marc-Jan, Catherine Li, and Boris Striepen. "High-Throughput Growth Assay for Toxoplasma gondii Using Yellow Fluorescent Protein." Antimicrobial Agents and Chemotherapy 47, no. 1 (January 2003): 309–16. http://dx.doi.org/10.1128/aac.47.1.309-316.2003.
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ABSTRACT A high-throughput growth assay for the protozoan parasite Toxoplasma gondii was developed based on a highly fluorescent transgenic parasite line. These parasites are stably transfected with a tandem yellow fluorescent protein (YFP) and are 1,000 times more fluorescent than the wild type. Parasites were inoculated in optical-bottom 384-well culture plates containing a confluent monolayer of host cells, and growth was monitored by using a fluorescence plate reader. The signal was linearly correlated with parasite numbers over a wide array. Direct comparison of the YFP growth assay with the β-galactosidase growth assay by using parasites expressing both reporters demonstrated that the assays' sensitivities were comparable but that the accuracy of the YFP assay was higher, especially at higher numbers of parasites per well. Determination of the 50%-inhibitory concentrations of three known growth-inhibiting drugs (cytochalasin D, pyrimethamine, and clindamycin) resulted in values comparable to published data. The delayed parasite death kinetics of clindamycin could be measured without modification of the assay, making this assay very versatile. Additionally, the temperature-dependent effect of pyrimethamine was assayed in both wild-type and engineered drug-resistant parasites. Lastly, the development of mycophenolic acid resistance after transfection of a resistance gene in T. gondii was followed. In conclusion, the YFP growth assay limits pipetting steps to a minimum, is highly versatile and amendable to automation, and should enable rapid screening of compounds to fulfill the need for more efficient and less toxic antiparasitic drugs.
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Hak, Muhammad Syafrudin, Masaaki Sasaguri, Farida Kamil Sulaiman, Enny Tyasandarwati Hardono, Akira Suzuki, Seiji Nakamura, and Masamichi Ohishi. "Longitudinal Study of Effect of Hotz's Plate and Lip Adhesion on Maxillary Growth in Bilateral Cleft Lip and Palate Patients." Cleft Palate-Craniofacial Journal 49, no. 2 (March 2012): 230–36. http://dx.doi.org/10.1597/10-042.
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Objective To investigate the effects of infant orthopedic treatment and lip adhesion on maxillary growth of patients with bilateral cleft lip and palate (BCLP). Design Prospective longitudinal study. Setting The present study was conducted at the Cleft Lip and Palate Center, Harapan Kita Children and Maternity Hospital, Indonesia, and the Department of Oral and Maxillofacial Surgery, Kyushu University Hospital, Japan. Subjects The study sample consisted of 53 patients with complete BCLP and 10 noncleft patients with other diseases. Patients with BCLP were divided into three groups: H (-), 11 patients treated without Hotz's plate; H (+), 24 treated with Hotz's plate; and LA-H, 18 treated with lip adhesion and Hotz's plate. Methods Serial dental casts were obtained from each BCLP child at the following four time points: first visit, labioplasty, palatoplasty, and 5 years of age. Each maxillary dental cast was scanned, and the linear and angular dimensions were measured. Results and Conclusion Lip adhesion showed a temporary negative effect. In all patients with BCLP, the surgeries affected the growth of the anterior arch width until the age of 5 years. Collapse of the premaxilla following labioplasty in the H (-) group affected the growth of dental arch length until the age of 5 years. Treatment using Hotz's plate prevented collapse of the premaxilla, and the growth of the arch length was comparable to that observed in the noncleft group.
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Reiss, Daniel, Michael Cappello, Lisa M. Harrison, and Richard Bungiro. "An Agar Plate Method for Culturing Hookworm Larvae: Analysis of Growth Kinetics and Infectivity Compared With Standard Coproculture Techniques." American Journal of Tropical Medicine and Hygiene 77, no. 6 (December 1, 2007): 1087–90. http://dx.doi.org/10.4269/ajtmh.2007.77.1087.
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Briggs, Michael D., Ella P. Dennis, Helen F. Dietmar, and Katarzyna A. Pirog. "New developments in chondrocyte ER-stress and related diseases." F1000Research 9 (April 24, 2020): 290. http://dx.doi.org/10.12688/f1000research.22275.1.
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Cartilage comprises a single cell type, the chondrocyte, embedded in a highly complex extracellular matrix. Disruption to the cartilage growth plate leads to reduced bone growth and results in a clinically diverse group of conditions known as genetic skeletal diseases (GSDs). Similarly, long-term degradation of articular cartilage can lead to osteoarthritis (OA), a disease characterised by joint pain and stiffness. As professionally secreting cells, chondrocytes are particularly susceptible to endoplasmic reticulum (ER) stress and this has been identified as a core disease mechanism in a group of clinically and pathologically related GSDs. If unresolved, ER stress can lead to chondrocyte cell death. Recent interest has focused on ER stress as a druggable target for GSDs and this has led to the first clinical trial for a GSD by repurposing an antiepileptic drug. Interestingly, ER stress markers have also been associated with OA in multiple cell and animal models and there is increasing interest in it as a possible therapeutic target for treatment. In summary, chondrocyte ER stress has been identified as a core disease mechanism in GSDs and as a contributory factor in OA. Thus, chondrocyte ER stress is a unifying factor for both common and rare cartilage-related diseases and holds promise as a novel therapeutic target.
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Heireman, Laura, Sofie Patteet, and Sophia Steyaert. "Performance of the new ID-fungi plate using two types of reference libraries (Bruker and MSI) to identify fungi with the Bruker MALDI Biotyper." Medical Mycology 58, no. 7 (February 6, 2020): 946–57. http://dx.doi.org/10.1093/mmy/myz138.
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Abstract During the last decade, matrix-assisted laser desorption ionization time-of-flight mass spectrometry (MALDI-TOF MS) has revolutionized the diagnosis of fungal infections. Recently, a new Conidia ID-fungi plate (IDFP) medium was introduced to facilitate growth and sampling of fungi. This study aimed to evaluate the IDFP for fungal MALDI-TOF MS identification by comparison with a standard fungal growth medium using two reference libraries. A total of 75 filamentous fungal isolates (including 32 dermatophytes) were inoculated on IDFP and Sabouraud-gentamicin-chloramphenicol (SGC) agar and identified by MALDI-TOF MS using formic acid/acetonitrile extraction. Both the commercially available Bruker library (version 2.0) and the public available MSI web application (version 2018) were applied. For 15% of the isolates, a faster growth was noticed on IDFP compared to SGC. IDFP enhanced the performance of fungal identification compared to SGC for both MSI (increase of 16% identifications to genus and 5% to species level) and Bruker library (increase of 22% identifications to genus and 8% to species level). In total, only 73% of the tested isolates were present in the Bruker library compared to 92% for MSI library. No significant difference (P = 0.46) in MALDI score between IDFP and SGC was observed for the MSI library, but scores were significantly (P = 0.03) higher for IDFP when using Bruker library, potentially explained by the prevention of agar contamination by using IDFP since the Bruker database was created from liquid media. IDFP is a promising alternative growth medium for MALDI-TOF MS fungal identification which would strongly benefit from optimizing the Bruker reference library.
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Gruppo, Veronica, Christine M. Johnson, Karen S. Marietta, Hataichanok Scherman, Erin E. Zink, Dean C. Crick, Linda B. Adams, Ian M. Orme, and Anne J. Lenaerts. "Rapid Microbiologic and Pharmacologic Evaluation of Experimental Compounds against Mycobacterium tuberculosis." Antimicrobial Agents and Chemotherapy 50, no. 4 (April 2006): 1245–50. http://dx.doi.org/10.1128/aac.50.4.1245-1250.2006.
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ABSTRACT The assessment of physiochemical and pharmacological properties at early stages of drug discovery can accelerate the conversion of hits and leads into candidates for further development. A strategy for streamlined evaluation of compounds against Mycobacterium tuberculosis in the early preclinical stage is presented in this report. As a primary assay to rapidly select experimental compounds with sufficient in vitro activity, the growth inhibition microtiter plate assay was devised as an alternative to current methods. This microdilution plate assay is a liquid culture method based on spectrophotometric readings of the bacillary growth. The performance of this method was compared to the performance of two established susceptibility methods using clinical available tuberculosis (TB) drugs. Data generated from all three assays were similar for all of the tested compounds. A second simple bioassay was devised to assess the oral bioavailability of compounds prior to extensive in vivo efficacy testing. The bioassay estimates drug concentrations in collected serum samples by a microdilution MIC plate method using M. tuberculosis. In the same assay, the MIC of the compound is also determined in the presence of 10% mouse serum as an indication of protein binding. The method was validated using different clinically available TB drugs, and results are discussed in this report. With these methodological advances, screening of compounds against tuberculosis in the preclinical phase will be rapid, can be adapted to semi-high-throughput screening, and will add relevant physicochemical and basic pharmacological criteria to the decision process of drug discovery.
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Bjelic, Dragana, Maja Ignjatov, Jelena Marinkovic, Nemanja Spremo, Maja Karaman, Zorica Nikolic, and Zarko Ivanovic. "Antifungal activity of indigenous Bacillus spp. isolated from soil." Zbornik Matice srpske za prirodne nauke, no. 133 (2017): 261–69. http://dx.doi.org/10.2298/zmspn1733261b.
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Biocontrol using plant growth-promoting rhizobacteria (PGPR) represents an alternative approach to disease management, since PGPR are known to promote growth and reduce diseases in various crops. Among the different PGPR, members of the genus Bacillus are prefered for most biotechnological uses due to their capability to form extremely resistant spores and produce a wide variety of metabolites with antimicrobial activity. The objective of this research was to identify antagonistic bacteria for management of the plant diseases. Eleven isolates of Bacillus spp. were obtained from the soil samples collected from different localities in the Province of Vojvodina. The antifungal activity of bacterial isolates against five fungal species was examined using a dual plate assay. Bacillus isolates exhibited the highest antifungal activity against Fusarium proliferatum, Fusarium oxysporum f. sp. cepae and Alternaria padwickii, while they had the least antagonistic effect on Fusarium verticillioides and Fusarium graminearum. Molecular identification showed that effective bacterial isolates were identified as Bacillus safensis (B2), Bacillus pumilus (B3, B11), Bacillus subtilis (B5, B7) and Bacillus megaterium (B8, B9). The highest antagonistic activity was exhibited by isolates B5 (from 39% to 62% reduction in fungal growth) and B7 (from 40% to 71% reduction in fungal growth). These isolates of B. subtilis could be used as potential biocontrol agents of plant diseases.
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Bull, James J., Bruce R. Levin, and Ian J. Molineux. "Promises and Pitfalls of In Vivo Evolution to Improve Phage Therapy." Viruses 11, no. 12 (November 21, 2019): 1083. http://dx.doi.org/10.3390/v11121083.
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Phage therapy is the use of bacterial viruses (phages) to treat bacterial infections, a medical intervention long abandoned in the West but now experiencing a revival. Currently, therapeutic phages are often chosen based on limited criteria, sometimes merely an ability to plate on the pathogenic bacterium. Better treatment might result from an informed choice of phages. Here we consider whether phages used to treat the bacterial infection in a patient may specifically evolve to improve treatment on that patient or benefit subsequent patients. With mathematical and computational models, we explore in vivo evolution for four phage properties expected to influence therapeutic success: generalized phage growth, phage decay rate, excreted enzymes to degrade protective bacterial layers, and growth on resistant bacteria. Within-host phage evolution is strongly aligned with treatment success for phage decay rate but only partially aligned for phage growth rate and growth on resistant bacteria. Excreted enzymes are mostly not selected for treatment success. Even when evolution and treatment success are aligned, evolution may not be rapid enough to keep pace with bacterial evolution for maximum benefit. An informed use of phages is invariably superior to naive reliance on within-host evolution.
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TOSHIMA, H., M. HACHIO, Y. IKEMOTO, J. OGASAWARA, A. HASE, K. TAKAHASHI, H. MASAKI, and Y. NISHIKAWA. "Prevalence of enteric bacteria that inhibit growth of enterohaemorrhagic Escherichia coli O157 in humans." Epidemiology and Infection 135, no. 1 (June 2, 2006): 110–17. http://dx.doi.org/10.1017/s0950268806006510.
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Enterohaemorrhagic Escherichia coli O157 (O157) is infectious to humans, particularly children, at very low doses and causes not only haemorrhagic colitis but also other serious symptoms. To investigate an association between intestinal bacterial flora and resistance to such infections, we screened faecal samples for the presence of enteric bacteria that are able to suppress the growth of O157. Samples from 303 individuals, 35 children (aged [les ]6 years) and 268 adults (aged 20–59 years), were examined. Colonies with different appearances on sorbitol MacConkey agar medium were screened for the production of bacteriocins inhibitory for O157 in an overlay agar plate assay. O157-inhibiting strains were isolated from 52 individuals. The prevalence of these bacteria tended to rise with age, and was significantly higher among 40- to 59-year-old adults (23/101, 22·8%) than among children (3/35, 8·6%; P<0·05). To test the hypothesis that these bacteriocin-producing strains contribute to resistance against O157 in human adults, we examined faecal samples of 25 healthy O157 carriers. Inhibitory bacteria were more prevalent among the latter (9/25, 36·0%) than among age-matched subjects who did not carry O157 (49/268, 18·3%). It appears, therefore, that inhibitory bacteria in the human gut may play a role in inhibiting propagation of O157 and/or suppressing expression of virulence factors by this pathogen.
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Kiso, Tetsuo, Ken-Ichi Fujita, Xu Ping, Toshio Tanaka, and Makoto Taniguchi. "Screening for Microtubule-Disrupting Antifungal Agents by Using a Mitotic-Arrest Mutant of Aspergillus nidulans and Novel Action of Phenylalanine Derivatives Accompanying Tubulin Loss." Antimicrobial Agents and Chemotherapy 48, no. 5 (May 2004): 1739–48. http://dx.doi.org/10.1128/aac.48.5.1739-1748.2004.
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ABSTRACT The microtubule, which is one of the major targets of anthelmintics, anticancer drugs, and fungicides, is composed mainly of α- and β-tubulins. We focused on a unique characteristic of an Aspergillus nidulans benA33 mutant to screen for microtubule-disrupting antifungal agents. This mutant, which has a β-tubulin with a mutation of a single amino acid, undergoes mitotic arrest due to the formation of hyperstable microtubules at 37°C. The heat sensitivity of the mutant is remedied by some antimicrotubule agents. We found that an agar plate assay with the mutant was able to distinguish three types of microtubule inhibitors. The growth recovery zones of the mutant were formed around paper disks containing microtubule inhibitors, including four benzimidazoles, ansamitocin P-3, griseofulvin, and rhizoxin, on the agar plate at 37°C. Nocodazole, thiabendazole, and griseofulvin reversed the mitotic arrest of the mutant and promoted its hyphal growth. Ansamitocin P-3 and rhizoxin showed growth recovery zones around the growth-inhibitory zones. Benomyl and carbendazim also reversed mitotic arrest but produced weaker growth recovery than the aforementioned drugs. Other microtubule inhibitors, such as colchicine, Colcemid, paclitaxel, podophyllotoxin, TN-16, vinblastine, and vincristine, as well as some cytoskeletal inhibitors tested, did not show such activity. In our screening, we newly identified two mycotoxins, citrinin and patulin, two sesquiterpene dialdehydes, polygodial and warburganal, and four phenylalanine derivatives, arphamenine A, l-2,5-dihydrophenylalanine (DHPA), N-tosyl-l-phenylalanine chloromethylketone, and N-carbobenzoxy-l-phenylalanine chloromethyl ketone. In a wild-type strain of A. nidulans, DHPA caused selective losses of microtubules, as determined by fluorescence microscopy, and of both α- and β-tubulins, as determined by Western blot analysis. This screening method involving the benA33 mutant of A. nidulans is useful, convenient, and highly selective. The phenylalanine derivatives tested are of a novel type of microtubule-disrupting antifungal agents, producing an accompanying loss of tubulins, and are different from well-known tubulin inhibitors affecting the assembly of tubulin dimers into microtubules.
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Hershberger, Ellie, and Michael J. Rybak. "Activities of Trovafloxacin, Gatifloxacin, Clinafloxacin, Sparfloxacin, Levofloxacin, and Ciprofloxacin against Penicillin-Resistant Streptococcus pneumoniae in an In Vitro Infection Model." Antimicrobial Agents and Chemotherapy 44, no. 3 (March 1, 2000): 598–601. http://dx.doi.org/10.1128/aac.44.3.598-601.2000.
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ABSTRACT We adapted an in vitro pharmacodynamic model of infection to incorporate infected fibrin clots. The bactericidal activities of various fluoroquinolones against two strains of penicillin-resistantStreptococcus pneumoniae were studied over a 48-h period. Bacteria were prepared in Muller-Hinton broth by using colonies from a 24-h tryptic soy agar plus 5% sheep blood plate and were added to a mixture of cryoprecipitate (80%) and thrombin (10%) to achieve approximately 106 CFU of organism per fibrin clot. The fibrin clots were suspended into the models and removed, in triplicate, at various time points over 48 h. Control models were also conducted to characterize the growth of S. pneumoniae in the growth medium without antibiotic. Trovafloxacin, gatifloxacin, clinafloxacin, sparfloxacin, levofloxacin, and ciprofloxacin were administered to simulate their pharmacokinetic profiles in humans. Fibrin clot samples were also plated onto antibiotic-containing tryptic soy agar plus 5% lysed horse blood to detect resistance. The newer fluoroquinolones demonstrated better activity than ciprofloxacin against both isolates. In conclusion, the newer quinolones demonstrated significant activity against penicillin-resistant S. pneumoniae, with standard dosing resulting in area under the concentration-time curve/MIC ratios and peak concentration/MIC ratios that resulted in 99.9% killing against these isolates.
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Smith, M. G. "Calculation of the expected increases of coliform organisms,Escherichia coliandSalmonella typhimurium, in raw blended mutton tissue." Epidemiology and Infection 99, no. 2 (October 1987): 323–31. http://dx.doi.org/10.1017/s0950268800067790.
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SUMMARYSamples of blended mutton tissue in small polyvinyl chloride sachets were incubated in water baths for different times and at varying temperatures. The temperature of each bath was recorded accurately throughout each experiment. Using equations previously derived for the lag and generation times of coliform organisms in blended mutton tissue, the expected increases of these bacteria were calculated from the time/temperature recordings. These were compared with the data obtained from plate counts made on the tissue samples in the sachets before and after incubation. The studies were done with a strain ofEscherichia coli, one ofSalmonella lyphimuriumand the coliform organisms naturally present on sheep carcasses processed in a commercial abattoir. The calculated growth agreed closely with that measured. Therefore, if mutton, after overnight chilling, is warmed again to temperatures within the growth range of these bacteria, the possible increases in the numbers of cells present can be calculated directly from time and temperature measurements.The implications for the present codes of practice in abattoirs are discussed.
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Pi, Rui, Qingyun Liu, Qi Jiang, and Qian Gao. "Characterization of linezolid-resistance-associated mutations in Mycobacterium tuberculosis through WGS." Journal of Antimicrobial Chemotherapy 74, no. 7 (April 23, 2019): 1795–98. http://dx.doi.org/10.1093/jac/dkz150.
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Abstract Objectives Linezolid is becoming an important antibiotic for treating MDR/XDR TB, but the mutations conferring resistance to linezolid remain inadequately characterized. Herein, we investigated the linezolid-resistance-associated mutations on a whole-genome scale through parallel selections of resistant isolates in vitro. Methods Ten parallel Mycobacterium tuberculosis H37Rv cultures were subjected to spontaneous mutant selection on 7H11 agar plates containing 2.5 mg/L linezolid. The linezolid resistance of resulting colonies was confirmed by growth on a second linezolid plate. WGS was then performed to identify mutations associated with linezolid resistance. Results Of 181 colonies appearing on the initial linezolid plates, 154 were confirmed to be linezolid resistant. WGS showed that 88.3% (136/154) of these isolates had a T460C mutation in rplC, resulting in a C154R substitution. The other 18 isolates harboured a single mutation in the rrl gene, with G2814T and G2270T mutations accounting for 7.8% (12/154) and 3.9% (6/154), respectively. Conclusions No mutations in novel genes were associated with linezolid resistance in a whole-genome investigation of 154 linezolid-resistant isolates selected in vitro. These results emphasize that rrl and rplC genes should be the major targets for molecular detection of linezolid resistance.
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Sohaskey, Charles D., and Alan G. Barbour. "Esterases in Serum-Containing Growth Media Counteract Chloramphenicol Acetyltransferase Activity In Vitro." Antimicrobial Agents and Chemotherapy 43, no. 3 (March 1, 1999): 655–60. http://dx.doi.org/10.1128/aac.43.3.655.
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ABSTRACT The spirochete Borrelia burgdorferi was unexpectedly found to be as susceptible to diacetyl chloramphenicol, the product of the enzyme chloramphenicol acetyltransferase, as it was to chloramphenicol itself. The susceptibilities of Escherichia coli and Bacillus subtilis, as well as that ofB. burgdorferi, to diacetyl chloramphenicol were then assayed in different media. All three species were susceptible to diacetyl chloramphenicol when growth media were supplemented with rabbit serum or, to a lesser extent, human serum. Susceptibility ofE. coli and B. subtilis to diacetyl chloramphenicol was not observed in the absence of serum, when horse serum was used, or when the rabbit or human serum was heated first. In the presence of 10% rabbit serum, a strain of E. colibearing the chloramphenicol acetyltransferase (cat) gene had a fourfold-lower resistance to chloramphenicol than in the absence of serum. A plate bioassay for chloramphenicol activity showed the conversion by rabbit, mouse, and human sera but not bacterial cell extracts or heated serum of diacetyl chloramphenicol to an inhibitory compound. Deacetylation of acetyl chloramphenicol by serum components was demonstrated by using fluorescent substrates and thin-layer chromatography. These studies indicate that esterases of serum can convert diacetyl chloramphenicol back to an active antibiotic, and thus, in vitro findings may not accurately reflect the level of chloramphenicol resistance by cat-bearing bacteria in vivo.
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Costa, Daniela, Rui M. Tavares, Paula Baptista, and Teresa Lino-Neto. "Cork Oak Endophytic Fungi as Potential Biocontrol Agents against Biscogniauxia mediterranea and Diplodia corticola." Journal of Fungi 6, no. 4 (November 14, 2020): 287. http://dx.doi.org/10.3390/jof6040287.
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An increase in cork oak diseases caused by Biscogniauxia mediterranea and Diplodia corticola has been reported in the last decade. Due to the high socio-economic and ecologic importance of this plant species in the Mediterranean Basin, the search for preventive or treatment measures to control these diseases is an urgent need. Fungal endophytes were recovered from cork oak trees with different disease severity levels, using culture-dependent methods. The results showed a higher number of potential pathogens than beneficial fungi such as cork oak endophytes, even in healthy plants. The antagonist potential of a selection of eight cork oak fungal endophytes was tested against B. mediterranea and D. corticola by dual-plate assays. The tested endophytes were more efficient in inhibiting D. corticola than B. mediterranea growth, but Simplicillium aogashimaense, Fimetariella rabenhorstii, Chaetomium sp. and Alternaria alternata revealed a high potential to inhibit the growth of both. Simplicillium aogashimaense caused macroscopic and microscopic mycelial/hyphal deformations and presented promising results in controlling both phytopathogens’ growth in vitro. The evaluation of the antagonistic potential of non-volatile and volatile compounds also revealed that A. alternata compounds could be further explored for inhibiting both pathogens. These findings provide valuable knowledge that can be further explored in in vivo assays to find a suitable biocontrol agent for these cork oak diseases.
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Höppner, Jakob, Katja Steff, Felix Lobert, Christoph M. Heyer, Berthold P. Hauffa, and Corinna Grasemann. "Rhizomelia and Impaired Linear Growth in a Girl with Juvenile Paget Disease: The Natural History of the Condition." Hormone Research in Paediatrics 94, no. 3-4 (2021): 151–58. http://dx.doi.org/10.1159/000517164.
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In ultra-rare bone diseases, information on growth during childhood is sparse. Juvenile Paget disease (JPD) is an ultra-rare disease, characterized by loss of function of osteoprotegerin (OPG). OPG inhibits osteoclast activation via the receptor activator of nuclear factor-κB (RANK) pathway. In JPD, overactive osteoclasts result in inflammatory-like bone disease due to grossly elevated bone resorption. Knowledge on the natural history of JPD, including final height and growth, is limited. Most affected children receive long-term antiresorptive treatment, mostly with bisphosphonates, to contain bone resorption, which may affect growth. In this study, we report the follow-up of height, growth velocity, and skeletal maturation in a 16-year-old female patient with JPD. The patient was treated with cyclic doses of pamidronate starting at 2.5 years of age and with 2 doses of denosumab at the age of 8 years, when pamidronate was paused. In the following years, a sustainable decline in a height <i>z</i>-score and a stunted pubertal growth spurt; despite appropriate maturation of the epiphyseal plates of the left hand, the proximal right humerus and both femora were observed. Whether this reflects the growth pattern in JPD or might be associated to the antiresorptive treatments is unclear, since there is very limited information available on the effect of bisphosphonates and denosumab on growth and the growth plate in pediatric patients. Studies are needed to understand the natural history of an ultra-rare bone disease and to assess the effects of antiresorptive treatment on the growing skeleton.
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Perugorria, Maria J., Ibone Labiano, Aitor Esparza-Baquer, Marco Marzioni, Jose J. G. Marin, Luis Bujanda, and Jesús M. Banales. "Bile Acids in Polycystic Liver Diseases: Triggers of Disease Progression and Potential Solution for Treatment." Digestive Diseases 35, no. 3 (2017): 275–81. http://dx.doi.org/10.1159/000450989.
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Polycystic liver diseases (PLDs) are a group of genetic hereditary cholangiopathies characterized by the development and progressive growth of cysts in the liver, which are the main cause of morbidity. Current therapies are based on surgical procedures and pharmacological strategies, which show short-term and modest beneficial effects. Therefore, the determination of the molecular mechanisms of pathogenesis appears to be crucial in order to find new potential targets for pharmacological therapy. Ductal plate malformation during embryogenesis and abnormal cystic cholangiocyte growth and secretion are some of the key mechanisms involved in the pathogenesis of PLDs. However, the discovery of the presence of bile acids in the fluid collected from human cysts and the intrahepatic accumulation of cytotoxic bile acids in an animal model of PLD (i.e. polycystic kidney (PCK) rat) suggest a potential role of impaired bile acid homeostasis in the pathogenesis of these diseases. On the other hand, ursodeoxycholic acid (UDCA) has emerged as a new potential therapeutic tool for PLDs by promoting the inhibition of cystic cholangiocyte growth in both PCK rats and highly symptomatic patients with autosomal dominant polycystic kidney disease (ADPKD: most common type of PLD), and improving symptoms. Chronic treatment with UDCA normalizes the decreased intracellular calcium levels in ADPKD human cholangiocytes in vitro, which results in the reduction of their baseline-stimulated proliferation. Moreover, UDCA decreases the liver concentration of cytotoxic bile acids in PCK rats and the bile acid-dependent enhanced proliferation of cystic cholangiocytes. Here, the role of bile acids in the pathogenesis of PLDs and the potential therapeutic value of UDCA for the treatment of these diseases are reviewed and future lines of investigation in this field are proposed.
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MacRae, V. E., T. Burdon, S. F. Ahmed, and C. Farquharson. "Ceramide inhibition of chondrocyte proliferation and bone growth is IGF-I independent." Journal of Endocrinology 191, no. 2 (November 2006): 369–77. http://dx.doi.org/10.1677/joe.1.06958.
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Proinflammatory cytokines inhibit growth plate development. However, their underlying mechanisms of action are unclear. These effects may be mediated by ceramide, a sphingosine-based lipid second messenger, which is elevated in a number of chronic inflammatory diseases. To test this hypothesis, we determined the effects of C2-ceramide, a cell permeable ceramide analogue, on the growth of the ATDC5 chondrogenic cell line and on cultured fetal mice metatarsals. In ATDC5 cells, C2-ceramide significantly induced apoptosis at both 40 (82%; P < 0.05) and 25 μM (53%; P < 0.05). At 40 μM, C2-ceramide significantly reduced proliferation ([3H]-thymidine uptake/mg protein) (62%; P < 0.05). C2-ceramide did not markedly alter the differentiation state of the cells as judged by the expression of markers of chondrogenesis and differentiation (sox 9, collagen II and collagen X). The IGF-I signalling pathway is the major autocrine/paracrine regulator of bone growth. Both in the presence and absence of IGF-I, C2-ceramide (25 μM) induced an equivalent reduction in proliferation (60%; P < 0.001). Similarly, C2-ceramide (40 μM) induced a 31% reduction in fetal metatarsal growth both in the presence and absence of IGF-I (both P < 0.001). Furthermore, C2-ceramide reduced ADCT5 proliferation in the presence of AG1024, an IGF-I and insulin receptor blocker. Therefore, C2-ceramide-dependent inhibition appears to be independent of IGF-mediated stimulation of bone growth. Indeed, biochemical studies demonstrated that C2-ceramide (25 μM) pretreatment did not alter IGF-I-stimulated phosphorylation of insulin receptor substrate-1, Akt or P44/42 MAP kinase. In conclusion, C2-ceramide inhibits proliferation and induces apoptosis in growth plate chondrocytes through an IGF-I independent mechanism.
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Johnson, Jacob D., Richard A. Dennull, Lucia Gerena, Miriam Lopez-Sanchez, Norma E. Roncal, and Norman C. Waters. "Assessment and Continued Validation of the Malaria SYBR Green I-Based Fluorescence Assay for Use in Malaria Drug Screening." Antimicrobial Agents and Chemotherapy 51, no. 6 (March 19, 2007): 1926–33. http://dx.doi.org/10.1128/aac.01607-06.
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ABSTRACT Several new fluorescence malaria in vitro drug susceptibility microtiter plate assays that detect the presence of malarial DNA in infected erythrocytes have recently been reported, in contrast to traditional isotopic screens that involve radioactive substrate incorporation to measure in vitro malaria growth inhibition. We have assessed and further characterized the malaria SYBR Green I-based fluorescence (MSF) assay for its ability to monitor drug resistance. In order to use the MSF assay as a drug screen, all assay conditions must be thoroughly examined. In this study we expanded upon the capabilities of this assay by including antibiotics and antifolates in the drug panel and testing folic acid-free growth conditions. To do this, we evaluated a more expansive panel of antimalarials in combination with various drug assay culture conditions commonly used in drug sensitivity screening for their activity against Plasmodium falciparum strains D6 and W2. The detection and quantitation limits of the MSF assay were 0.04 to 0.08% and ∼0.5% parasitemia, respectively. The MSF assay quality was significantly robust, displaying a Z′ range of 0.73 to 0.95. The 50% inhibitory concentrations for each drug and culture condition combination were determined by using the MSF assay. Compared to the standard [3H]hypoxanthine assay, the MSF assay displayed the expected parasite drug resistance patterns with a high degree of global and phenotypic correlation (r 2 ≥ 0.9238), regardless of which culture condition combination was used. In conclusion, the MSF assay allows for reliable one-plate high-throughput, automated malaria in vitro susceptibility testing without the expense, time consumption, and hazard of other screening assays.
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Shin, Sung Jae, and Michael T. Collins. "Thiopurine Drugs Azathioprine and 6-Mercaptopurine Inhibit Mycobacterium paratuberculosis Growth In Vitro." Antimicrobial Agents and Chemotherapy 52, no. 2 (December 10, 2007): 418–26. http://dx.doi.org/10.1128/aac.00678-07.
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ABSTRACT The in vitro susceptibility of human- and bovine-origin Mycobacterium paratuberculosis to the thioupurine drugs 6-mercaptopurine (6-MP) and azathioprine (AZA) was established using conventional plate counting methods and the MGIT 960 ParaTB culture system. Both 6-MP and AZA had antibacterial activity against M. paratuberculosis; isolates from Crohn's disease patients tended to be more susceptible than were bovine-origin isolates. Isolates of Mycobacterium avium, used as controls, were generally resistant to both AZA and 6-MP, even at high concentrations (≥64.0 μg/ml). Among rapidly growing mycobacteria, Mycobacterium phlei was susceptible to 6-MP and AZA whereas Mycobacterium smegmatis strains were not. AZA and 6-MP limited the growth of, but did not kill, M. paratuberculosis in a dose-dependent manner. Anti-inflammatory drugs in the sulfonamide family (sulfapyridine, sulfasalazine, and 5-aminosalycilic acid [mesalamine]) had little or no antibacterial activity against M. paratuberculosis. The conventional antibiotics azithromycin and ciprofloxacin, used as control drugs, were bactericidal for M. paratuberculosis, exerting their killing effects on the organism relatively quickly. Simultaneous exposure of M. paratuberculosis to 6-MP and ciprofloxacin resulted in significantly higher CFU than use of ciprofloxacin alone. These data may partially explain the paradoxical response of Crohn's disease patients infected with M. paratuberculosis to treatment with immunosuppressive thiopurine drugs, i.e., they do not worsen with anti-inflammatory treatment as would be expected with a microbiological etiologic pathogen. These findings also should influence the design of therapeutic trials to evaluate antibiotic treatments of Crohn's disease: AZA drugs may confound interpretation of data on therapeutic responses for both antibiotic-treated and control groups.
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Hasan, Akhmad Endang Zainal, I. Made Artika, and Syaeful Abidin. "Produksi Asam Laktat dan Pola Pertumbuhan Bakteri Asam Laktat dengan Pemberian Dosis Rendah Propolis Trigona spp asal Pandeglang Indonesia." Current Biochemistry 1, no. 3 (November 25, 2016): 126–35. http://dx.doi.org/10.29244/cb.1.3.126-135.
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Propolis is known to have an antimicrobial activity and can prevent various diseases. Propolis consumption is feared to have negative impact on the activity of digestive lactid acid bacteria (LAB). The aim of this research was to examine the effect of propolis on the growth and lactic acid production of three LAB. Ethanol Extraction Propolis (EEP) concentrations examined were control, eep and X propolis 0% (control), 0.2%, 0.6%, 1.0% and X propolis at 0.4% concentration. The parameters analyzed were the growth of bacteria counted with Total Plate Count (TPC) method and lactic acid production using titrable acidity analysis. Propolis at 0,6% concentration stimulated the growth of Lactobacillus casei subsp. rhamnosus (LCR, 24.725x108 cell/mL), but inhibited the average lactic acid production (0.071%) lower than control (0,149%). Propolis did not affect the growth of Streptococcus thermophillus (STP), but propolis at 0,6% concentration stimulated lactic acid production (0.182%) higher than control (0.112%). Propolis inhibited the growth of Lactobacillus delbrueckii subsp. bulgaricus (LDB), but at 0,2% concentration, its population was still highest (3.775x108 cell/mL) and lactic acid production was stimulated (0.195%) higher than control (0.123%).
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Turovskiy, Yevgeniy, Thomson Cheryian, Ammar Algburi, Ruth E. Wirawan, Paul Takhistov, Patrick J. Sinko, and Michael L. Chikindas. "Susceptibility ofGardnerella vaginalisBiofilms to Natural Antimicrobials Subtilosin,ε-Poly-L-Lysine, and Lauramide Arginine Ethyl Ester." Infectious Diseases in Obstetrics and Gynecology 2012 (2012): 1–9. http://dx.doi.org/10.1155/2012/284762.
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Bacterial vaginosis is a common vaginal infection associated with numerous gynecological and obstetric complications. This condition is characterized by the presence of thick adherent vaginal biofilms, composed mainly ofGardnerella vaginalis. This organism is thought to be the primary aetiological cause of the infection paving the way for various opportunists to colonize the niche. Previously, we reported that the natural antimicrobials subtilosin,ε-poly-L-lysine, and lauramide arginine ethyl ester selectively inhibit the growth of this pathogen. In this study, we used plate counts to evaluate the efficacy of these antimicrobials against established biofilms ofG. vaginalis. Additionally, we validated and compared two rapid methods (ATP viability and resazurin assays) for the assessment of cell viability in the antimicrobial-treatedG. vaginalisbiofilms. Out of the tested antimicrobials, lauramide arginine ethyl ester had the strongest bactericidal effect, followed by subtilosin, with clindamycin and polylysine showing the weakest effect. In comparison to plate counts, ATP viability and resazurin assays considerably underestimated the bactericidal effect of some antimicrobials. Our results indicate that these assays should be validated for every new application.
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Bang, C., A. Schilhabel, K. Weidenbach, A. Kopp, T. Goldmann, T. Gutsmann, and R. A. Schmitz. "Effects of Antimicrobial Peptides on Methanogenic Archaea." Antimicrobial Agents and Chemotherapy 56, no. 8 (May 14, 2012): 4123–30. http://dx.doi.org/10.1128/aac.00661-12.
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ABSTRACTAs members of the indigenous human microbiota found on several mucosal tissues,Methanobrevibacter smithiiandMethanosphaera stadtmanaeare exposed to the effects of antimicrobial peptides (AMPs) secreted by these epithelia. Although antimicrobial and molecular effects of AMPs on bacteria are well described, data for archaea are not available yet. Besides, it is not clear whether AMPs affect them as the archaeal cell envelope differs profoundly in terms of chemical composition and structure from that of bacteria. The effects of different synthetic AMPs on growth ofM. smithii,M. stadtmanae, andMethanosarcina mazeiwere tested using a microtiter plate assay adapted to their anaerobic growth requirements. All three tested methanoarchaea were highly sensitive against derivatives of human cathelicidin, of porcine lysin, and a synthetic antilipopolysaccharide peptide (Lpep); however, sensitivities differed markedly among the methanoarchaeal strains. The potent AMP concentrations affecting growth were below 10 μM, whereas growth ofEscherichia coliWBB01 was not affected at peptide concentrations up to 10 μM under the same anaerobic growth conditions. Atomic force microscopy and transmission electron microscopy revealed that the structural integrity of the methanoarchaeal cells is destroyed within 4 h after incubation with AMPs. The disruption of the cell envelope ofM. smithii,M. stadtmanae, andM. mazeiwithin a few minutes of exposure was verified by using LIVE/DEAD staining. Our results strongly suggest that the release of AMPs by eukaryotic epithelial cells is a potent defense mechanism targeting not only bacteria, but also methanoarchaea.
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Whaley, Sarah G., Sarah Tsao, Sandra Weber, Qing Zhang, Katherine S. Barker, Martine Raymond, and P. David Rogers. "TheRTA3Gene, Encoding a Putative Lipid Translocase, Influences the Susceptibility of Candida albicans to Fluconazole." Antimicrobial Agents and Chemotherapy 60, no. 10 (August 1, 2016): 6060–66. http://dx.doi.org/10.1128/aac.00732-16.
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ABSTRACTTheRTA3gene, coding for a member of the Rta1p-like lipid-translocating exporter family, is coordinately upregulated with the ATP-binding cassette transporter genesCDR1andCDR2in azole-resistant clinical isolates ofCandida albicansthat carry activating mutations in the transcription factor Tac1p. We show here that deletingRTA3in an azole-resistant clinical isolate carrying a Tac1p-activating mutation lowered fluconazole resistance by 2-fold, while overexpressingRTA3in an azole-susceptible clinical isolate resulted in enhanced fluconazole tolerance associated with trailing growth in a liquid microtiter plate assay. We also demonstrate that an Rta3p-green fluorescent protein (GFP) fusion protein localizes predominantly to the plasma membrane, consistent with a putative function for Rta3p as a lipid translocase.
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Stenholm, Teppo, Antti J. Hakanen, Jonne Vaarno, Sari Pihlasalo, Perttu Terho, Pekka E. Hänninen, Jaana Vuopio-Varkila, Pentti Huovinen, and Pirkko Kotilainen. "Methicillin-Resistant Staphylococcus aureus Screening by Online Immunometric Monitoring of Bacterial Growth under Selective Pressure." Antimicrobial Agents and Chemotherapy 53, no. 12 (September 14, 2009): 5088–94. http://dx.doi.org/10.1128/aac.00518-09.
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ABSTRACT Rapid, high-throughput screening tools are needed to contain the spread of hospital-acquired methicillin (meticillin)-resistant Staphylococcus aureus (MRSA) strains. Most techniques used in current clinical practice still require time-consuming culture for primary isolation of the microbe. We present a new phenotypic assay for MRSA screening. The technique employs a two-photon excited fluorescence (TPX) detection technology with S. aureus-specific antibodies that allows the online monitoring of bacterial growth in a single separation-free process. Different progressions of fluorescence signals are recorded for methicillin-susceptible and -resistant strains when the growth of S. aureus is monitored in the presence of cefoxitin. The performance of the new technique was evaluated with 20 MRSA strains, 6 methicillin-susceptible S. aureus strains, and 7 coagulase-negative staphylococcal strains and two different monoclonal S. aureus-specific antibodies. When either of these antibodies was used, the sensitivity and the specificity of the TPX assay were 100%. All strains were correctly classified within 8 to 12 h, and up to 70 samples were simultaneously analyzed on a single 96-well microtiter plate. As a phenotypic method, the TPX assay is suited for screening purposes. The final definition of methicillin resistance in any S. aureus strain should be based on the presence of the mecA gene. The main benefit afforded by the initial use of the TPX methodology lies in its low cost and applicability to high-throughput analysis.
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Staines, K. A., A. S. Pollard, I. M. McGonnell, C. Farquharson, and A. A. Pitsillides. "Cartilage to bone transitions in health and disease." Journal of Endocrinology 219, no. 1 (August 19, 2013): R1—R12. http://dx.doi.org/10.1530/joe-13-0276.
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Aberrant redeployment of the ‘transient’ events responsible for bone development and postnatal longitudinal growth has been reported in some diseases in what is otherwise inherently ‘stable’ cartilage. Lessons may be learnt from the molecular mechanisms underpinning transient chondrocyte differentiation and function, and their application may better identify disease aetiology. Here, we review the current evidence supporting this possibility. We firstly outline endochondral ossification and the cellular and physiological mechanisms by which it is controlled in the postnatal growth plate. We then compare the biology of these transient cartilaginous structures to the inherently stable articular cartilage. Finally, we highlight specific scenarios in which the redeployment of these embryonic processes may contribute to disease development, with the foresight that deciphering those mechanisms regulating pathological changes and loss of cartilage stability will aid future research into effective disease-modifying therapies.
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Janaki, T. "BIOCONTROL OF FUSARIUM OXYSPORUM IN UNSTERILIZED SOIL BY NOVEL STREPTOMYCES CACAOI SUBSP CACAOI [M20]." International Journal of Pharmacy and Pharmaceutical Sciences 9, no. 3 (February 3, 2017): 78. http://dx.doi.org/10.22159/ijpps.2017v9i3.16579.
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Objective: To find bio fungicide from mangrove actinomycetes for controlling seed and soil borne pathogen-Fusarium oxysporum. Methods: A total of 25 actinomycetes were isolated by pour plate method. These were screened for fungicidal activity by agar plug method. The isolate M20 was characterised further for identification. The phytotoxicity study was done; biocontrol of Fusarium oxysporum with 10% culture filtrate was done using food poisoning technique. Volatile toxicity of isolate M20 was studied by inverted plate technique. The methanolic crude extract was subjected for UV–Vis spectral analysis for identifying the group of compound present.Results: The isolated M20 found to be better in antifungal activity. 10% culture filtrate actively inhibited the growth of Fusarium oxysporum (77.7%), 10% culture filtrate was taken as a standard concentration for biocontrol of Fusarium oxysporum using green gram as the test plants. The 15th-day green gram plants under treatment with the antagonist (A), antagonist+pathogen (A+P), antagonist+pathogen+rhizobium (A+P+R) yielded high biomass and better growth. The disease development by the pathogen in green gram was controlled by the antagonist. The compounds (pyrimidine nucleosides-neutral and acidic polyoxins (230 nm), (270-290 nm) and heptaene antifungal antibiotics (406-417 nm)) are preliminarily confirmed from the methanolic crude extract of the isolate M20-Streptomyces cacaoi subsp cacaoi.Conclusion: Since the isolate M20 controlled the growth and disease causing potentiality of Fusarium oxysporum, it can be effectively used to control seed and soil borne diseases that are caused by Fusarium oxysporum.
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Simsa-Maziel, Stav, and Efrat Monsonego-Ornan. "Interleukin-1β Promotes Proliferation and Inhibits Differentiation of Chondrocytes through a Mechanism Involving Down-Regulation of FGFR-3 and p21." Endocrinology 153, no. 5 (April 4, 2012): 2296–310. http://dx.doi.org/10.1210/en.2011-1756.
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The proinflammatory cytokine IL-1β is elevated in many childhood chronic inflammatory diseases as well as obesity and can be associated with growth retardation. Here we show that IL-1β affects bone growth by directly disturbing the normal sequence of events in the growth plate, resulting in increased proliferation and widening of the proliferative zone, whereas the hypertrophic zone becomes disorganized, with impaired matrix structure and increased apoptosis and osteoclast activity. This was also evident in vitro: IL-1β increased proliferation and caused a G1-to-S phase shift in the cell cycle in ATDC5 chondrocytes, accompanied by a reduction in fibroblast growth factor receptor-3 (FGFR-3) and its downstream gene, the cell-cycle inhibitor p21 and its family member p57, whereas the cell-cycle promoter E2F-2 was increased. The reduction in FGFR-3, p21, and p57 was followed by delayed cell differentiation, manifested by decreases in proteoglycan synthesis, mineralization, alkaline phosphatase activity, and the expression of Sox9, RunX2, collagen type II, collagen type X, and other matrix proteins. Taken together, we suggest that IL-1β alters normal chondrogenesis and bone growth through a mechanism involving down-regulation of FGFR-3 and p21.
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Malkoski, Marina, Stuart G. Dashper, Neil M. O'Brien-Simpson, Gert H. Talbo, Mary Macris, Keith J. Cross, and Eric C. Reynolds. "Kappacin, a Novel Antibacterial Peptide from Bovine Milk." Antimicrobial Agents and Chemotherapy 45, no. 8 (August 1, 2001): 2309–15. http://dx.doi.org/10.1128/aac.45.8.2309-2315.2001.
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ABSTRACT Caseinomacropeptide (CMP) is a heterogeneous C-terminal fragment (residues 106 to 169) of bovine milk κ-casein composed of glycosylated and phosphorylated forms of different genetic variants. We have demonstrated that CMP has growth-inhibitory activity against the oral opportunistic pathogens Streptococcus mutans andPorphyromonas gingivalis and against Escherichia coli. CMP was fractionated using reversed-phase high-performance liquid chromatography (RP-HPLC), and each fraction was tested for activity against S. mutans in a 96-well-plate broth assay. Fractions were characterized by N-terminal sequence analysis and mass spectrometry. The active form of CMP was shown to be the nonglycosylated, phosphorylated κ-casein (residues 106 to 169) [κ-casein(106–169)], which we have designated kappacin. Endoproteinase Glu-C was used to hydrolyze CMP, and the generated peptides were separated using RP-HPLC and gel filtration-HPLC and then tested for activity against S. mutans. The peptide Ser(P)149κ-casein-A(138–158) was the only peptide generated by endoproteinase Glu-C digestion that exhibited growth-inhibitory activity. Peptides corresponding to the sequences of the inhibitory peptide Ser(P)149κ-casein-A(138–158) and its nonphosphorylated counterpart κ-casein-A(138–158) were chemically synthesized and tested for antibacterial activity. The synthetic Ser(P)149 κ-casein-A(138–158) displayed growth-inhibitory activity against S. mutans(MIC, 59 μg/ml [26 μM]). The nonphosphorylated peptide, however, did not inhibit growth at the concentrations tested, indicating that phosphorylation is essential for activity.
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Frazier, Kendall S. "Drug-induced Physeal Abnormalities in Preclinical Toxicity Studies." Toxicologic Pathology 45, no. 7 (June 23, 2017): 869–75. http://dx.doi.org/10.1177/0192623317713319.
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Most toxic physeal changes are characterized microscopically by altered chondrocyte development, proliferation, or maturation in the growth plate and eventually result in disordered appositional bone growth. Many therapeutic drugs directly or indirectly target proteins involved in chondrocytic differentiation and maturation pathways, so toxic physeal injury has become increasingly common in preclinical toxicologic pathology. While physeal dysplasia has been associated with several different drug classes including bisphosphonates, vascular endothelial growth factor receptor inhibitors, fibroblast growth factor receptor inhibitors, transforming growth factor beta receptor inhibitors, and vascular targeting agents, physeal changes often share similar morphologic features including thickening and disorganization of the hypertrophic layer, increased numbers of hypertrophic chondrocytes, altered mineralization of endochondral ossification, and/or increased thickness of subphyseal bone. Knowledge of genetic and nutritional diseases affecting bone growth has been important in helping to determine which specific target drugs may be affecting that could result in toxic physeal lesions. A pathophysiologic mechanism for most physeal toxicants has been determined in detail using a variety of investigative techniques. However, due to the signaling cross talk and the tight regulation required for chondrocyte maturation in the physis, several growth factor pathways are likely to be affected simultaneously with pharmacologic disruption of physeal homeostasis and inhibition of one factor necessary for chondrocyte function often affects others.
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Bouillon, Roger, Geert Carmeliet, Lieve Verlinden, Evelyne van Etten, Annemieke Verstuyf, Hilary F. Luderer, Liesbet Lieben, Chantal Mathieu, and Marie Demay. "Vitamin D and Human Health: Lessons from Vitamin D Receptor Null Mice." Endocrine Reviews 29, no. 6 (October 1, 2008): 726–76. http://dx.doi.org/10.1210/er.2008-0004.
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Abstract The vitamin D endocrine system is essential for calcium and bone homeostasis. The precise mode of action and the full spectrum of activities of the vitamin D hormone, 1,25-dihydroxyvitamin D [1,25-(OH)2D], can now be better evaluated by critical analysis of mice with engineered deletion of the vitamin D receptor (VDR). Absence of a functional VDR or the key activating enzyme, 25-OHD-1α-hydroxylase (CYP27B1), in mice creates a bone and growth plate phenotype that mimics humans with the same congenital disease or severe vitamin D deficiency. The intestine is the key target for the VDR because high calcium intake, or selective VDR rescue in the intestine, restores a normal bone and growth plate phenotype. The VDR is nearly ubiquitously expressed, and almost all cells respond to 1,25-(OH)2D exposure; about 3% of the mouse or human genome is regulated, directly and/or indirectly, by the vitamin D endocrine system, suggesting a more widespread function. VDR-deficient mice, but not vitamin D- or 1α-hydroxylase-deficient mice, and man develop total alopecia, indicating that the function of the VDR and its ligand is not fully overlapping. The immune system of VDR- or vitamin D-deficient mice is grossly normal but shows increased sensitivity to autoimmune diseases such as inflammatory bowel disease or type 1 diabetes after exposure to predisposing factors. VDR-deficient mice do not have a spontaneous increase in cancer but are more prone to oncogene- or chemocarcinogen-induced tumors. They also develop high renin hypertension, cardiac hypertrophy, and increased thrombogenicity. Vitamin D deficiency in humans is associated with increased prevalence of diseases, as predicted by the VDR null phenotype. Prospective vitamin D supplementation studies with multiple noncalcemic endpoints are needed to define the benefits of an optimal vitamin D status.
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Dharmaputra, Okky Setyawati, Lisdar Idwan Sudirman, and Evarini Anna Ratnaningsih. "Mikobiota pada Buah Pisang Kultivar Lampung untuk Pengendalian Hayati Fusarium semitectum." Jurnal Fitopatologi Indonesia 14, no. 1 (September 20, 2018): 30. http://dx.doi.org/10.14692/jfi.14.1.30.
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Fusarium semitectum is a pathogenic fungus causing fruit rot of banana fruits. Biological control agents have been used as an alternative to control postharvest diseases. The objective of this study was to test antagonistic potential of mycobiota of banana fruits (Musa cuminata cultivar Lampung) against F. semitectum BIO 91055. The tested fungi were isolated from healthy banana cultivar Lampung collected from Gembrong market located in Bogor using serial dilution method, followed by pour plate method. Test of antagonism activity was carried out using dual culture method. Seventeen fungal isolates were isolated, they consisted of 14 filamentous fungal isolates and 3 yeast isolates. Four filamentous fungal isolates inhibited the growth of F. semitectum BIO 91055 more than 70%, they were Aspergillus niger, Cercosporella sp., Plectosphaerella sp., and Trichoderma hamatum. Three isolates (Cercosporella sp., Plectosphaerella sp., and Trichoderma hamatum) did not cause any diseases of banana fruits and they were considered as potential biocontrol agents.
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Malik, Muhammad, Kalyan Chavda, Xilin Zhao, Nirali Shah, Syed Hussain, Natalia Kurepina, Barry N. Kreiswirth, Robert J. Kerns, and Karl Drlica. "Induction of Mycobacterial Resistance to Quinolone Class Antimicrobials." Antimicrobial Agents and Chemotherapy 56, no. 7 (May 7, 2012): 3879–87. http://dx.doi.org/10.1128/aac.00474-12.
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ABSTRACTAn agar plate assay was developed for detecting the induction of drug-resistant mycobacterial mutants during exposure to inhibitors of DNA gyrase. WhenMycobacterium smegmatison drug-containing agar, resistant colonies arose over a period of 2 weeks. ArecAdeficiency reduced mutant recovery, consistent with involvement of the SOS response in mutant induction. The C-8-methoxy compounds gatifloxacin and moxifloxacin allowed the recovery of fewer resistant mutants than either ciprofloxacin or levofloxacin when present at the same multiple of the MIC; a quinolone-like 8-methoxy-quinazoline-2,4-dione was more effective at restricting the emergence of resistant mutants than its cognate fluoroquinolone. Thus, the structure of fluoroquinolone-like compounds affects mutant recovery. A spontaneous mutator mutant ofM. smegmatis, obtained by growth in medium containing both isoniazid and rifampin, increased mutant induction during exposure to ciprofloxacin. Moreover, the mutator increased the size of spontaneous resistant mutant subpopulations, as detected by population analysis. Induction of ciprofloxacin resistance was also observed withMycobacterium tuberculosisH37Rv. When measured with clinical isolates, no difference in mutant recovery was observed between multidrug-resistant (MDR) and pansusceptible isolates. This finding is consistent with at least some MDR isolates ofM. tuberculosislacking mutators detectable by the agar plate assay. Collectively, the data indicate that the use of fluoroquinolones against tuberculosis may induce resistance and that the choice of quinolone may be important for restricting the recovery of induced mutants.
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Maitra, Arundhati, Dimitrios Evangelopoulos, Alina Chrzastek, Liam T. Martin, Aidan Hanrath, Ellie Chapman, Helen C. Hailes, et al. "Carprofen elicits pleiotropic mechanisms of bactericidal action with the potential to reverse antimicrobial drug resistance in tuberculosis." Journal of Antimicrobial Chemotherapy 75, no. 11 (August 13, 2020): 3194–201. http://dx.doi.org/10.1093/jac/dkaa307.
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Abstract Background The rise of antimicrobial drug resistance in Mycobacterium tuberculosis coupled with the shortage of new antibiotics has elevated TB to a major global health priority. Repurposing drugs developed or used for other conditions has gained special attention in the current scenario of accelerated drug development for several global infectious diseases. In a similar effort, previous studies revealed that carprofen, a non-steroidal anti-inflammatory drug, selectively inhibited the growth of replicating, non-replicating and MDR clinical isolates of M. tuberculosis. Objectives We aimed to reveal the whole-cell phenotypic and transcriptomic effects of carprofen in mycobacteria. Methods Integrative molecular and microbiological approaches such as resazurin microtitre plate assay, high-throughput spot-culture growth inhibition assay, whole-cell efflux inhibition, biofilm inhibition and microarray analyses were performed. Analogues of carprofen were also synthesized and assessed for their antimycobacterial activity. Results Carprofen was found to be a bactericidal drug that inhibited mycobacterial drug efflux mechanisms. It also restricted mycobacterial biofilm growth. Transcriptome profiling revealed that carprofen likely acts by targeting respiration through the disruption of membrane potential. The pleiotropic nature of carprofen’s anti-TB action may explain why spontaneous drug-resistant mutants could not be isolated in practice. Conclusions This immunomodulatory drug and its chemical analogues have the potential to reverse TB antimicrobial drug resistance, offering a swift path to clinical trials of novel TB drug combinations.
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Ganim, Christine, Mustafa Mazher, and Erin Breaker. "Establishment of a Sink Gallery to Investigate Growth of Carbapenemase-Producing Klebsiella pneumoniae and Biofilms in P-Traps." Infection Control & Hospital Epidemiology 41, S1 (October 2020): s219—s220. http://dx.doi.org/10.1017/ice.2020.763.
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Background: Hand-hygiene sink drains in healthcare facilities may provide an environment for the survival and dissemination of various multidrug-resistant organisms (MDROs), including carbapenemase-producing Klebsiella pneumoniae (CPKP). We developed a sink model system to establish and test native drinking water biofilms containing CPKP in the p-traps of hand-hygiene sink drains. Methods: A handwashing sink gallery was designed to consist of 6-wall mounted stainless-steel sink basins connected to the same municipal water line. Each sink’s plumbing included a chrome-plated brass p-trap. Healthcare facility conditions were simulated to include handwashing events with the addition of hand-soap and municipal water 4 per day, and nutritional shake (simulating liquid waste) 1 per day. Resultant biofilms in the p-traps of each sink were harvested after 28 days for community analysis. Microbial community analyses were performed on selected biofilm samples using 16S rRNA sequencing of the V4 hypervariable region of genomic DNA. Another experiment evaluated 28-day p-trap biofilm inoculated with CPKP CAV1016 (10 mL 7.010E 7 CFU/mL) and was assessed over 14 days. Heterotrophic plate counts (HPCs) were determined on R2A medium (7 days of incubation at 25C). CPKP was quantified on mEndo selective medium (48 hours of incubation at 36C). Results: Biofilms developed in all p-traps, but biofilm HPC (5.78 mean log CFU/cm2, range 4.35–7.16) and community diversity (15–20 genera per p-trap) varied with sink position. Community analysis showed similarities in bacterial community composition and diversity between sinks 1 and 2, and between sinks 3, 5 and 6, but with differences between the 2 groups. The most abundant family in sinks 3, 5, and 6 was Erythrobacteriaceae (76%, 78%, and 55% of the total reads, respectively), whereas sinks 1 and 2 were dominated by Sphingomonadaceae (63% and 36%) and Methylobacteriaceae (19% and 55%). Also, 16S sequencing revealed the presence of potential opportunistic pathogens in the biofilms, including reads attributed to Pseudomonas and Acinetobacter. CPKP CAV1016 inoculated into 28-day p-trap biofilms colonized and persisted in all 6 sinks for 12 days after inoculation. Conclusions: Despite all 6 sinks sharing an incoming water line, soap, and carbon and energy source, there was a significant variation in the bacterial community composition observed between the sinks. CPKP can colonize and persist in the p-trap biofilms; however, additional work is needed to achieve a reproducible model system. Once this is achieved, the sink gallery will be used to investigate interventions to mitigate colonization or persistence of CPKP in p-trap biofilms.Funding: NoneDisclosures: None
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de Cózar, Cristina, Iván Caballero, Gonzalo Colmenarejo, Laura M. Sanz, Emilio Álvarez-Ruiz, Francisco-Javier Gamo, and Concepción Cid. "Development of a Novel High-Density [3H]Hypoxanthine Scintillation Proximity Assay To Assess Plasmodium falciparum Growth." Antimicrobial Agents and Chemotherapy 60, no. 10 (July 25, 2016): 5949–56. http://dx.doi.org/10.1128/aac.00433-16.
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ABSTRACTThe discovery and development of new antimalarial drugs are becoming imperative because of the spread of resistance to current clinical treatments. The lack of robustly validated antimalarial targets and the difficulties with the building in of whole-cell activity in screening hits are hampering target-based approaches. However, phenotypic screens of structurally diverse molecule libraries are offering new opportunities for the identification of novel antimalarials. Several methodologies can be used to determine the whole-cellin vitropotencies of antimalarial hits. The [3H]hypoxanthine incorporation assay is considered the “gold standard” assay for measurement of the activity of antimalarial compounds against intraerythrocytic forms ofPlasmodium falciparum. However, the method has important limitations, as the assay is not amenable for high-throughput screening since it remains associated with the 96-well plate format. We have overcome this drawback by adapting the [3H]hypoxanthine incorporation method to a 384-well high-density format by coupling a homogeneous scintillation proximity assay (SPA) and thus eliminating the limiting filtration step. This SPA has been validated using a diverse set of 1,000 molecules, including both a representative set from the Tres Cantos Antimalarial Set (TCAMS) of compounds and molecules inactive against whole cells. The results were compared with those from theP. falciparumlactate dehydrogenase whole-cell assay, another method that is well established as a surrogate for parasite growth and is amenable for high-throughput screening. The results obtained demonstrate that the SPA-based [3H]hypoxanthine incorporation assay is a suitable design that is adaptable to high-throughput antimalarial drug screening and that maintains the features, robustness, and reliability of the standard filtration hypoxanthine incorporation method.
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Xu, Jianping, Chiatogu Onyewu, Heather J. Yoell, Rabia Y. Ali, Rytas J. Vilgalys, and Thomas G. Mitchell. "Dynamic and Heterogeneous Mutations to Fluconazole Resistance in Cryptococcus neoformans." Antimicrobial Agents and Chemotherapy 45, no. 2 (February 1, 2001): 420–27. http://dx.doi.org/10.1128/aac.45.2.420-427.2001.
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ABSTRACT Infections with the human pathogenic basidiomycetous yeastCryptococcus neoformans are often treated with fluconazole. Resistance to this antifungal agent has been reported. This study investigated the patterns of mutation to fluconazole resistance inC. neoformans in vitro. The MIC of fluconazole was measured for 21 strains of C. neoformans. The MICs for these 21 strains differed (0.25 to 4.0 μg/ml), but the strains were selected for this study because they exhibited no growth on plates of yeast morphology agar (YMA) containing 8 μg of fluconazole per ml. To determine their mutation rates, six independent cultures from a single original colony were established for each of the 21 strains. Each culture was then spread densely on a YMA plate with 8 μg of fluconazole per ml. A random set of putative mutants was subcultured, and the MIC of fluconazole was determined for each mutant. The 21 strains evinced significant heterogeneity in their mutation rates. The MICs of the putative mutants ranged widely, from their original MIC to 64 μg of fluconazole per ml. However, for this set of 21 strains, there was no significant correlation between the original MIC for a strain and the mutation rate of that strain; the MIC for the mutant could not be predicted from the original MIC. These results suggest that dynamic and heterogeneous mutational processes are involved in generating fluconazole resistance in C. neoformans.
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Nahdah, Fauziyyah, Noorkomala Sari, Akhmad Rizali, and Rabiatul Wahdah. "Antagonisme Fungi Endofit Daun Jarak Pagar (Jatropha curcas) terhadap Fusarium oxysporum C2 Penyebab Busuk Umbi pada Bawang Merah in Vitro." Agrotechnology Research Journal 4, no. 1 (June 25, 2020): 47. http://dx.doi.org/10.20961/agrotechresj.v4i1.41351.
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<p class="Abstract">Basal plate rot is a major disease on shallot caused by <em>Fusarium oxysporum</em>. Endophytic fungi is promising to use as antagonist agent to the pathogen. Endophyte is microbes that are living in plant cells and have an asymptomatic characteristic. Nowadays, fungal endophyte is believed to produce antimicrobial substances similar with their plant host's natural product. <em>Jatropha curcas</em> is one of the plants containing secondary metabolites that have antifungal activities. The research aimed to study the ability of endophyte from <em>Jatropha curcas</em> to inhibit the growth of <em>Fusarium oxysporum</em>. The dual culture method was used in this research and the data were analyzed by SPSS software. This antagonism test was conducted by 9 isolates endophyte and each plate consisted of 3 replicates. The result revealed endophyte fungal obtaining 9 isolates with the radial growth of 4,5 cm/2 days. Endophytes of <em>Jatropha curcas</em> L. were able to inhibit the growth of <em>Fusarium oxysporum</em> C2. The percentage of inhibition of <em>Fusarium oxysporum </em>causing of root blight diseases was controlled by up 38.27 - 74.48%. The highest percentage of inhibition is gained by B4b and the lowest of it is A2b. Our observations showed that each endophyte has a consistent linear trend. B4b still leaded as the highest strength to inhibit the growth of pathogen on the monitoring of 3, 5, and 7 days. Moreover, the ability of fungi endophyte from <em>Jatropha curcas</em> as antagonist agent to <em>Fusarium oxysporum</em> needs to be further examined by the in vivo method.</p>
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Wu, Meng-Chuan, Ying-Chun Chen, Tzu-Lung Lin, Pei-Fang Hsieh, and Jin-Town Wang. "Cellobiose-Specific Phosphotransferase System of Klebsiella pneumoniae and Its Importance in Biofilm Formation and Virulence." Infection and Immunity 80, no. 7 (May 7, 2012): 2464–72. http://dx.doi.org/10.1128/iai.06247-11.
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ABSTRACTKlebsiella pneumoniaeis a Gram-negative bacillus belonging to the familyEnterobacteriaceae. In the past 20 years,K. pneumoniaehas become the predominant pathogen causing community-acquired pyogenic liver abscess (PLA). The formation of biofilm facilitates bacterial colonization and has been implicated in reduced susceptibility to the host immune response. To investigate genes related to biofilm formation in a PLA-associatedK. pneumoniaestrain, a transposon mutant library was screened by microtiter plate assay to identify isolates impaired for biofilm formation. One of the mutants was disrupted incelB, encoding the putative cellobiose-specific subunit IIC of enzyme II (EIIC) of a carbohydrate phosphotransferase system (PTS). This transmembrane protein is responsible for recognizing and binding specific sugars and transporting them across the cell membrane into the cytoplasm. Deletion and chromosomal complementation ofcelBconfirmed, by microtiter plate and slide culture assays, thatcelBwas indeed responsible for biofilm formation. Cellobiose-specific PTS activities of deletion mutants grown in LB broth and 0.005% cellobiose minimal medium were markedly lower than that of the wild-type strain grown under the same conditions, thereby confirming the involvement ofcelBin cellobiose transport. In 0.005% cellobiose minimal medium, thecelBmutant showed a delay in growth compared to the wild-type strain. In a mouse model of intragastric infection, deletion of thecelBgene increased the survival rate from 12.5% to 87.5%, which suggests that thecelBdeletion mutant also exhibited reduced virulence. Thus, thecelBlocus ofK. pneumoniae may contribute to biofilm formation and virulence through the metabolism of cellobiose.