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Artykuły w czasopismach na temat "Periodontal disease Molecular aspects"
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AS, Dr Maniyammai, Dr Amudha M, Dr Renuka Devi R, Dr Esther Nalini H, and Dr Arun Kumar Prasad. "Adaptive immune response: Molecular aspects of periodontal disease." International Journal of Applied Dental Sciences 7, no. 4 (October 1, 2021): 89–92. http://dx.doi.org/10.22271/oral.2021.v7.i4b.1356.
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Tsuchida, Sachio. "Proteome Analysis of Molecular Events in Oral Pathogenesis and Virus: A Review with a Particular Focus on Periodontitis." International Journal of Molecular Sciences 21, no. 15 (July 22, 2020): 5184. http://dx.doi.org/10.3390/ijms21155184.
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Some systemic diseases are unquestionably related to periodontal health, as periodontal disease can be an extension or manifestation of the primary disease process. One example is spontaneous gingival bleeding, resulting from anticoagulant treatment for cardiac diseases. One important aspect of periodontal therapy is the care of patients with poorly controlled disease who require surgery, such as patients with uncontrolled diabetes. We reviewed research on biomarkers and molecular events for various diseases, as well as candidate markers of periodontal disease. Content of this review: (1) Introduction, (2) Periodontal disease, (3) Bacterial and viral pathogens associated with periodontal disease, (4) Stem cells in periodontal tissue, (5) Clinical applications of mass spectrometry using MALDI-TOF-MS and LC-MS/MS-based proteomic analyses, (6) Proteome analysis of molecular events in oral pathogenesis of virus in GCF, saliva, and other oral Components in periodontal disease, (7) Outlook for the future and (8) Conclusions. This review discusses proteome analysis of molecular events in the pathogenesis of oral diseases and viruses, and has a particular focus on periodontitis.
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Lin, Peiya, Hiromi Niimi, Yujin Ohsugi, Yosuke Tsuchiya, Tsuyoshi Shimohira, Keiji Komatsu, Anhao Liu, et al. "Application of Ligature-Induced Periodontitis in Mice to Explore the Molecular Mechanism of Periodontal Disease." International Journal of Molecular Sciences 22, no. 16 (August 18, 2021): 8900. http://dx.doi.org/10.3390/ijms22168900.
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Periodontitis is an inflammatory disease characterized by the destruction of the periodontium. In the last decade, a new murine model of periodontitis has been widely used to simulate alveolar bone resorption and periodontal soft tissue destruction by ligation. Typically, 3-0 to 9-0 silks are selected for ligation around the molars in mice, and significant bone loss and inflammatory infiltration are observed within a week. The ligature-maintained period can vary according to specific aims. We reviewed the findings on the interaction of systemic diseases with periodontitis, periodontal tissue destruction, the immunological and bacteriological responses, and new treatments. In these studies, the activation of osteoclasts, upregulation of pro-inflammatory factors, and excessive immune response have been considered as major factors in periodontal disruption. Multiple genes identified in periodontal tissues partly reflect the complexity of the pathogenesis of periodontitis. The effects of novel treatment methods on periodontitis have also been evaluated in a ligature-induced periodontitis model in mice. This model cannot completely represent all aspects of periodontitis in humans but is considered an effective method for the exploration of its mechanisms. Through this review, we aimed to provide evidence and enlightenment for future studies planning to use this model.
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Teng, Y. T. A. "Protective and Destructive Immunity in the Periodontium: Part 2—T-cell-mediated Immunity in the Periodontium." Journal of Dental Research 85, no. 3 (March 2006): 209–19. http://dx.doi.org/10.1177/154405910608500302.
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Based on the results of recent research in the field and Part 1 of this article (in this issue), the present paper will discuss the protective and destructive aspects of the T-cell-mediated adaptive immunity associated with the bacterial virulent factors or antigenic determinants during periodontal pathogenesis. Attention will be focused on: (i) osteoimmunology and periodontal disease; (ii) some molecular techniques developed and applied to identify critical microbial virulence factors or antigens associated with host immunity (with Actinobacillus actinomycetemcomitans and Porphyromonas gingivalis as the model species); and (iii) summarizing the identified virulence factors/antigens associated with periodontal immunity. Thus, further understanding of the molecular mechanisms of the host’s T-cell-mediated immune responses and the critical microbial antigens related to disease pathogenesis will facilitate the development of novel therapeutics or protocols for future periodontal treatments. Abbreviations used in the paper are as follows: A. actinomycetemcomitans ( Aa), Actinobacillus actinomycetemcomitans; Ab, antibody; DC, dendritic cells; mAb, monoclonal antibody; pAb, polyclonal antibody; OC, osteoclast; PAMP, pathogen-associated molecular patterns; P. gingivalis ( Pg), Porphyromonas gingivalis; RANK, receptor activator of NF-κB; RANKL, receptor activator of NF-κB ligand; OPG, osteoprotegerin; TCR, T-cell-receptors; TLR, Toll-like receptors.
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Teng, Y. T. A. "Protective and Destructive Immunity in the Periodontium: Part 1—Innate and Humoral Immunity and the Periodontium." Journal of Dental Research 85, no. 3 (March 2006): 198–208. http://dx.doi.org/10.1177/154405910608500301.
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Based on the results of recent research in the field, the present paper will discuss the protective and destructive aspects of the innate vs. adaptive (humoral and cell-mediated) immunity associated with the bacterial virulent factors or antigenic determinants during periodontal pathogenesis. Attention will be focused on: (i) the Toll-like receptors (TLR), the innate immune repertoire for recognizing the unique molecular patterns of microbial components that trigger innate and adaptive immunity for effective host defenses, in some general non-oral vs. periodontal microbial infections; (ii) T-cell-mediated immunity, Th-cytokines, and osteoclastogenesis in periodontal disease progression; and (iii) some molecular techniques developed and used to identify critical microbial virulence factors or antigens associated with host immunity (using Actinobacillus actinomycetemcomitans and Porphyromonas gingivalis as the model species). Therefore, further understanding of the molecular interactions and mechanisms associated with the host’s innate and adaptive immune responses will facilitate the development of new and innovative therapeutics for future periodontal treatments. Abbreviations used in the paper are as follows: A. actinomycetemcomitans ( Aa), Actinobacillus actinomycetemcomitans; Ab, antibody; DC, dendritic cells; mAb, monoclonal antibody; pAb, polyclonal antibody; PAMP, pathogen-associated molecular patterns; P. gingivalis ( Pg), Porphyromonas gingivalis; and TLR, Toll-like receptors.
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Divaris, K. "Searching Deep and Wide: Advances in the Molecular Understanding of Dental Caries and Periodontal Disease." Advances in Dental Research 30, no. 2 (October 21, 2019): 40–44. http://dx.doi.org/10.1177/0022034519877387.
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During the past decades, remarkable progress has been made in the understanding of the molecular basis of the 2 most common oral diseases, dental caries and periodontal disease. Improvements in our knowledge of the diseases’ underlying biology have illuminated previously unrecognized aspects of their pathogenesis. Importantly, the key role of the oral (supragingival and subgingival) microbiome is now well recognized, and both diseases are now best understood as dysbiotic. From a host susceptibility standpoint, some progress has been made in dissecting the “hyperinflammatory” trait and other pathways of susceptibility underlying periodontitis, and novel susceptibility loci have been reported for dental caries. Nevertheless, there is a long road to the translation of these findings and the realization of precision oral health. There is promise and hope that the rapidly increasing capacity of generating multiomics data layers and the aggregation of study samples and cohorts comprising thousands of participants will accelerate the discovery and translation processes. A first key element in this process has been the identification and interrogation of biologically informed disease traits—these “deep” or “precise” traits have the potential of revealing biologically homogeneous disease signatures and genetic susceptibility loci that might present with overlapping or heterogeneous clinical signs. A second key element has been the formation of international consortia with the goals of combining and harmonizing oral health data of thousands of individuals from diverse settings—these “wide” collaborative approaches leverage the power of large sample sizes and are aimed toward the discovery or validation of genetic influences that would otherwise be impossible to detect. Importantly, advancements via these directions require an unprecedented engagement of systems biology and team science models. The article highlights novel insights into the molecular basis of dental caries and chronic periodontitis that have been gained from recent and ongoing studies involving “deep” and “wide” analytical approaches.
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Elmallawany, Marwa A., Marwa Ahmed EL-Dardiry, Reham K. Nahnoush, Mohamed Akmal, Adam A. Afife, and Mohamed S. Badr. "Structural and Genetic Diversity of Entamoeba gingivalis Trophozoites Isolated from Diseased and Healthy Periodontal Sites." Open Access Macedonian Journal of Medical Sciences 10, A (February 25, 2022): 661–67. http://dx.doi.org/10.3889/oamjms.2022.8713.
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BACKGROUND: At present, there is little documented about the variability aspects of Entamoeba gingivalis (E. gingivalis) in relation to periodontal diseases. This is perhaps due to several specialists rejecting the notion that E. gingivalis can cause periodontal disease. AIM: The aim of the present study was to compare the morphological and genetic variability within trophozoites isolated from diseased (n = 26) and healthy periodontal sites (n = 14). METHODS: Detailed microscopic analyses were performed, in addition to post real-time polymerase chain reaction 18S-SSU rRNA gene scanning technology, using reference synthetic genes to analyze melting curve features from different isolates. RESULTS: All trophozoites isolated from diseased sites were significantly larger in size than those isolated from healthy sites. In addition, they were found in clusters, containing many leukophagocytosis and in a significantly higher number than those from healthy sites. Gene scanning revealed diversity within the isolates with a significantly higher number of mutant forms (18 out of 26) within the trophozoites isolated from diseased sites, 14 of them were of unknown origin. Four melting curves matched E. gingivalis H57 strain and the remaining eight were related to the wild strain (ATCC-30927). Isolates from healthy sites corresponded to the wild type (12 out of 14) with only two related to H57 strain. CONCLUSION: The study confirmed morphological and genetic variability between different isolates; We still recommend further in-depth molecular studies to investigate the role of this oral protozoan in the pathogenicity of periodontal affection. The study highlighted the importance of real engagement of multidisciplinary diagnostic strategies, involving experts from variable medical fields to reach truthful scientific outcomes concerning the association of certain microorganism to particular diseases or disorders.
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Elgezawi, Moataz, Rasha Haridy, Khalid Almas, Moamen A. Abdalla, Omar Omar, Hatem Abuohashish, Abeer Elembaby, Uta Christine Wölfle, Yasir Siddiqui, and Dalia Kaisarly. "Matrix Metalloproteinases in Dental and Periodontal Tissues and Their Current Inhibitors: Developmental, Degradational and Pathological Aspects." International Journal of Molecular Sciences 23, no. 16 (August 11, 2022): 8929. http://dx.doi.org/10.3390/ijms23168929.
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Objectives: This review article aims to describe some of the roles of Matrix metalloproteinases (MMPs) in enamel, dentine, dental caries, hybrid layer degradation, pulp and periodontal tissues, throwing light on their current inhibitors. The article addresses the potential of MMPs to serve as biomarkers with diagnostic and therapeutic value. Design: The sections of this review discuss MMPs’ involvement in developmental, remodeling, degradational and turnover aspects of dental and periodontal tissues as well as their signals in the pathogenesis, progress of different lesions and wound healing of these tissues. The literature was searched for original research articles, review articles and theses. The literature search was conducted in PubMed and MEDLINE for articles published in the last 20 years. Results: 119 published papers, two textbooks and two doctoral theses were selected for preparing the current review. Conclusions: MMPs are significant proteases, of evident contribution in dental and periapical tissue development, health and disease processes, with promising potential for use as diagnostic and prognostic disease biomarkers. Continuing understanding of their role in pathogenesis and progress of different dental, periapical and periodontal lesions, as well as in dentine-pulp wound healing could be a keystone to future diagnostic and therapeutic regimens.
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Dieterle, Martin Philipp, Ayman Husari, Thorsten Steinberg, Xiaoling Wang, Imke Ramminger, and Pascal Tomakidi. "From the Matrix to the Nucleus and Back: Mechanobiology in the Light of Health, Pathologies, and Regeneration of Oral Periodontal Tissues." Biomolecules 11, no. 6 (May 31, 2021): 824. http://dx.doi.org/10.3390/biom11060824.
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Among oral tissues, the periodontium is permanently subjected to mechanical forces resulting from chewing, mastication, or orthodontic appliances. Molecularly, these movements induce a series of subsequent signaling processes, which are embedded in the biological concept of cellular mechanotransduction (MT). Cell and tissue structures, ranging from the extracellular matrix (ECM) to the plasma membrane, the cytosol and the nucleus, are involved in MT. Dysregulation of the diverse, fine-tuned interaction of molecular players responsible for transmitting biophysical environmental information into the cell’s inner milieu can lead to and promote serious diseases, such as periodontitis or oral squamous cell carcinoma (OSCC). Therefore, periodontal integrity and regeneration is highly dependent on the proper integration and regulation of mechanobiological signals in the context of cell behavior. Recent experimental findings have increased the understanding of classical cellular mechanosensing mechanisms by both integrating exogenic factors such as bacterial gingipain proteases and newly discovered cell-inherent functions of mechanoresponsive co-transcriptional regulators such as the Yes-associated protein 1 (YAP1) or the nuclear cytoskeleton. Regarding periodontal MT research, this review offers insights into the current trends and open aspects. Concerning oral regenerative medicine or weakening of periodontal tissue diseases, perspectives on future applications of mechanobiological principles are discussed.
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Srimaneepong, Viritpon, Artak Heboyan, Muhammad Sohail Zafar, Zohaib Khurshid, Anand Marya, Gustavo V. O. Fernandes, and Dinesh Rokaya. "Fixed Prosthetic Restorations and Periodontal Health: A Narrative Review." Journal of Functional Biomaterials 13, no. 1 (February 1, 2022): 15. http://dx.doi.org/10.3390/jfb13010015.
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Periodontal health plays an important role in the longevity of prosthodontic restorations. The issues of comparative assessment of prosthetic constructions are complicated and not fully understood. The aim of this article is to review and present the current knowledge regarding the various technical, clinical, and molecular aspects of different prosthetic biomaterials and highlight the interactions between periodontal health and prosthetic restorations. Articles on periodontal health and fixed dental prostheses were searched using the keywords “zirconium”, “CAD/CAM”, “dental ceramics”, “metal–ceramics”, “margin fit”, “crown”, “fixed dental prostheses”, “periodontium”, and “margin gap” in PubMed/Medline, Scopus, Google Scholar, and Science Direct. Further search criteria included being published in English, and between January 1981 and September 2021. Then, relevant articles were selected, included, and critically analyzed in this review. The margin of discrepancy results in the enhanced accumulation of dental biofilm, microleakage, hypersensitivity, margin discoloration, increased gingival crevicular fluid flow (GCF), recurrent caries, pulp infection and, lastly, periodontal lesion and bone loss, which can lead to the failure of prosthetic treatment. Before starting prosthetic treatment, the condition of the periodontal tissues should be assessed for their oral hygiene status, and gingival and periodontal conditions. Zirconium-based restorations made from computer-aided design and computer-aided manufacturing (CAD/CAM) technology provide better results, in terms of marginal fit, inflammation reduction, maintenance, and the restoration of periodontal health and oral hygiene, compared to constructions made by conventional methods, and from other alloys. Compared to subgingival margins, supragingival margins offer better oral hygiene, which can be maintained and does not lead to secondary caries or periodontal disease.
Rozprawy doktorskie na temat "Periodontal disease Molecular aspects"
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Gully, Neville. "Studies on the growth and metabolism of Eikenella corrodens /." Title page, summary and table of contents only, 2000. http://web4.library.adelaide.edu.au/theses/09PH/09phg973.pdf.
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Irani, Dilshad Minocher. "Role of the surface associated material of Eikenella corrodens in bone resorption associated with periodontal disease : a research thesis submitted in fulfilment of the requirements for the degree of Master of Science in Dentistry." Title page, contents and summary only, 1998. http://web4.library.adelaide.edu.au/theses/09DSM/09dsmi65.pdf.
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Mooney, John. "Molecular and cellular aspects of the humoral immune response in periodontal disease and other related conditions." Thesis, University of Glasgow, 1996. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.321510.
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Kennedy, Rebekah Storm. "Microbiological and immunological aspects of equine periodontal disease." Thesis, University of Glasgow, 2017. http://theses.gla.ac.uk/8064/.
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Periodontal disease is a common and painful condition in the horse. Although awareness of the condition is growing amongst the veterinary profession and horse owners, the presence of the disease is often overlooked and treatment can be difficult. Despite this, there have been few recent studies of the aetiopathogenesis of the condition. Certain species of bacteria may act as periodontal pathogens, stimulating a destructive inflammatory response in periodontal tissues and this has been well recognised as being important to the aetiopathogenesis of the disease in man. However few equine studies on this aspect of the disease have been carried out. The main aims of this study were: - 1) to identify the bacteria associated with a healthy oral cavity and periodontitis in horses using culture dependent and independent methods; 2) to assess the differences in bacterial populations between the healthy and periodontitis groups and identify putative pathogens; 3) to quantify the expression patterns of TLRs 2, 4 and 9, the pro-inflammatory cytokines IL-1β and TNFα, anti-inflammatory cytokine IL-10 and Th1/Th2/Th17 cytokines IL-4, IL-6/ IL-12, IFNɣ/ IL-17, within gingival tissue from each sample group; 4) to use matched data to establish if associations exist between the presence and quantity of bacterial species present and TLR expression and 5) to determine activation of TLRs 2, 4 and 9 by putative pathogens using specific in- vitro TLR assays. Swabs were taken from the gingival sulcus of 42 orally healthy horses and plaque samples were taken from the periodontal pockets of 61 horses with periodontal disease. The location and grade of the lesion was noted and an equine dental chart completed for each case. Bacteria were identified using high throughput 16S rRNA gene sequencing, QPCR, whole genome sequencing and conventional culture followed by 16S gene sequencing. Gingival biopsies were taken from 13 orally healthy horses and 20 horses with periodontitis and gene expression of TLR 2, TLR 4, TLR 9, IL-1β, IL-4, IL-6, IL-10, IL-12, IL-17, TNFα and IFNɣ was measured. THP-1X Blue, MyD88 THP-1X Blue, HEK hTLR 2 Blue and HEK hTLR 4 Blue human cell lines were co-cultured with putative periodontal pathogens and their response measured via level of secreted embryonic alkaline phosphatase. Clinical, microbiological and immunological data underwent cross-matching analysis. Microbial populations showed 89% dissimilarly between oral health and periodontitis with a less diverse population present in diseased equine periodontal pockets. The most discriminative bacteria between health and disease identified at genus level were Fusobacteria and Acinetobacter in health and Pseudomonas and Prevotella in periodontitis. The most abundant genera were Gemella (36.5%), Pseudomonas (14%) and Acinetobacter (8%) in orally healthy samples and Pseudomonas (25%), Prevotella (14%) and Acinetobacter (9.4%) in periodontitis samples. Whole genome sequencing revealed the presence of 75 species of Prevotella in the equine oral cavity and a significantly higher number of reads corresponding to Prevotella bivia, Prevotella dentalis, Prevotella denticola, Prevotella intermedia, Prevotella melaninogenica, Prevotella nigrescens were noted in diseased samples. Significant increases in expression of TLR 4 mRNA, TLR 9 mRNA and, in particular TLR 2, mRNA were noted in diseased equine gingival tissue in addition to increased pro-inflammatory and anti-inflammatory cytokine mRNA expression. Presence of P. intermedia was significantly positively correlated with expression of TLR 2 in equine periodontitis. In addition, the presence of Aggregatibacter actinomycetemcomitans was positively associated with disease severity and expression of TLR 4 mRNA in the horse. Co-culture of periodontal pathogens with human cell lines revealed that the innate immune response to the presence of these bacteria is mainly mediated through TLR 2 activation. The use of both culture dependent and culture independent methods to investigate the equine oral microbiome has provided significant breadth and depth of information on the microbiology of equine periodontal disease. Microbial populations are significantly different as expected and bacteria belonging to the Prevotella genus have been strongly implicated in the aetiopathogenesis of the condition. The innate immune response produced in periodontally diseased equine gingival tissue has been characterised for the first time in the horse.
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Ng, Kwai-sang Sam, and 吳桂生. "Psychological perspectives of periodontal disease." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2005. http://hub.hku.hk/bib/B36918210.
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Preber, Hans. "Cigarette smoking and periodontal disease clinical and therapeutic aspects /." Stockholm : Dept. of Periodontology, Karolinska Institutet, 1986. http://books.google.com/books?id=4ulpAAAAMAAJ.
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Porter, S. R. "Immunological aspects of rapidly progressive periodontitis." Thesis, University of Bristol, 1987. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.377350.
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Sörgjerd, Karin. "Molecular Aspects of Transthyretin Amyloid Disease." Doctoral thesis, Linköpings universitet, Biokemi, 2008. http://urn.kb.se/resolve?urn=urn:nbn:se:liu:diva-12566.
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This thesis was made to get a deeper understanding of how chaperones interact with unstable, aggregation prone, misfolded proteins involved in human disease. Over the last two decades, there has been much focus on misfolding diseases within the fields of biochemistry and molecular biotechnology research. It has become obvious that proteins that misfold (as a consequence of a mutation or outer factors), are the cause of many diseases. Molecular chaperones are proteins that have been defined as agents that help other proteins to fold correctly and to prevent aggregation. Their role in the misfolding disease process has been the subject for this thesis. Transthyretin (TTR) is a protein found in human plasma and in cerebrospinal fluid. It works as a transport protein, transporting thyroxin and holo-retinol binding protein. The structure of TTR consists of four identical subunits connected through hydrogen bonds and hydrophobic interactions. Over 100 point mutations in the TTR gene are associated with amyloidosis often involving peripheral neurodegeneration (familial amyloidotic polyneuropathy (FAP)). Amyloidosis represents a group of diseases leading to extra cellular deposition of fibrillar protein known as amyloid. We used human SH-SY5Y neuroblastoma cells as a model for neurodegeneration. Various conformers of TTR were incubated with the cells for different amounts of time. The experiments showed that early prefibrillar oligomers of TTR induced apoptosis when neuroblastoma cells were exposed to these species whereas mature fibrils were not cytotoxic. We also found increased expression of the molecular chaperone BiP in cells challenged with TTR oligomers. Point mutations destabilize TTR and result in monomers that are unstable and prone to aggregate. TTR D18G is naturally occurring and the most destabilized TTR mutant found to date. It leads to central nervous system (CNS) amyloidosis. The CNS phenotype is rare for TTR amyloid disease. Most proteins associated with amyloid disease are secreted proteins and secreted proteins must pass the quality control check within the endoplasmic reticulum (ER). BiP is a Hsp70 molecular chaperone situated in the ER. BiP is one of the most important components of the quality control system in the cell. We have used TTR D18G as a model for understanding how an extremely aggregation prone protein is handled by BiP. We have shown that BiP can selectively capture TTR D18G during co-expression in both E. coli and during over expression in human 293T cells and collects the mutant in oligomeric states. We have also shown that degradation of TTR D18G in human 293T cells occurs slower in presence of BiP, that BiP is present in amyloid deposition in human brain and mitigates cytotoxicity of TTR D18G oligomers.<br>Denna avhandling handlar om proteiner. Särskilt de som inte fungerar som de ska utan har blivit vad man kallar ”felveckade”. Anledningen till att proteiner veckas fel beror ofta (men inte alltid) på mutationer i arvsmassan. Felveckade proteiner kan leda till sjukdomar hos människor och djur (man brukar tala om amyloidsjukdomar), ofta av neurologisk karaktär. Exempel på amyloidsjukdomar är polyneuropati, där perifera nervsystemet är drabbat, vilket leder till begränsad rörelseförmåga och senare till förlamning; och Alzheimer´s sjukdom, där centrala nervsystemet är drabbat och leder till begränsad tankeförmåga och minnesförluster. Studierna som presenteras i denna avhandling har gått ut på att få en bättre förståelse för hur felveckade proteiner interagerar med det som vi har naturligt i cellerna och som fungerar som skyddande, hjälpande proteiner, så kallade chaperoner. Transtyretin (TTR) är ett protein som cirkulerar i blodet och transporterar tyroxin (som är ett hormon som bland annat har betydelse för ämnesomsättningen) samt retinol-bindande protein (vitamin A). I TTR genen har man funnit över 100 punktmutationer, vilka har kopplats samman med amyloidsjukdomar, bland annat ”Skellefteåsjukan”. Mutationer i TTR genen leder ofta till att proteinet blir instabilt vilket leder till upplösning av TTR tetrameren till monomerer. Dessa monomerer kan därefter sammanfogas på nytt men denna gång på ett sätt som är farligt för organismen. I denna avhandling har fokus legat på en mutation som kallas TTR D18G, vilken har identifierats i olika delar av världen och leder till en dödlig form av amyloidos i centrala nervsystemet. Det chaperon som vi har studerat benämns BiP och är beläget i en cellkomponent som kallas för det endoplasmatiska retiklet (ER). I ER finns cellens kontrollsystem i vilket det ses till att felveckade proteiner inte släpps ut utan istället bryts ned. Denna avhandling har visat att BiP kan fånga upp TTR D18G inuti celler och där samla mutanten i lösliga partiklar som i detta fall är ofarliga för cellen. Avhandligen har också visat att nedbrytningen av TTR D18G sker mycket långsammare när BiP finns i riklig mängd.
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Boström, Lennart. "Tobacco smoking and periodontal disease : some clinical, microbiological and immunological aspects /." Stockholm, 2000. http://diss.kib.ki.se/2000/91-628-4456-3/.
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Hanley, Shirley Anne. "Molecular characterisation of an immunodominant 55kDa surface antigen of Porphyromonas gingivalis W50." Thesis, Queen Mary, University of London, 1998. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.312824.
Pełny tekst źródłaKsiążki na temat "Periodontal disease Molecular aspects"
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Sampath, Narayanan A., ed. Biology of the periodontal connective tissues. Chicago: Quintessence Pub. Co., 1998.
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European Symposium on the Borderland Between Caries and Periodontal Disease. (4th 1990 Geneva, Switzerland). Application of molecular science to caries and periodontal disease: 4th European Symposium of Borderland Between Caries and Periodontal Disease, Geneva, Switzerland, 25-26 January, 1990. Oxford: Pergamon, 1990.
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Saleh, Mazen T. Molecular aspects of infectious disease. New York: Nova Science Publishers, 2011.
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W, Gorrod J., Albano O, and Papa S, eds. Molecular aspects of human disease. Chichester: E. Horwood, 1989.
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Preber, Hans. Cigarette smoking and periodontal disease: Clinical and therapeutical aspects. [S.l: s.n.], 1986.
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Junya, Kobayashi, and SpringerLink (Online service), eds. Genetic Variants in Periodontal Health and Disease. Berlin, Heidelberg: Springer-Verlag Berlin Heidelberg, 2010.
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Gokhale, David Anand. Molecular genetic aspects of Hodgkin's disease. Manchester: University of Manchester, 1996.
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Parker, Jane, ed. Molecular Aspects of Plant Disease Resistance. Oxford, UK: Wiley-Blackwell, 2008. http://dx.doi.org/10.1002/9781444301441.
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1960-, Parker Jane, ed. Molecular aspects of plant disease resistance. Ames, Iowa: Blackwell, 2008.
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1954-, Wiggs Janey L., ed. Molecular genetics of ocular disease. New York: Wiley-Liss, 1995.
Znajdź pełny tekst źródłaCzęści książek na temat "Periodontal disease Molecular aspects"
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Braun-Falco, Markus, Henry J. Mankin, Sharon L. Wenger, Markus Braun-Falco, Stephan DiSean Kendall, Gerard C. Blobe, Christoph K. Weber, et al. "Periodontal Diseases." In Encyclopedia of Molecular Mechanisms of Disease, 1620–21. Berlin, Heidelberg: Springer Berlin Heidelberg, 2009. http://dx.doi.org/10.1007/978-3-540-29676-8_1396.
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Dumitrescu, Alexandrina L., and Masashi Tanaka. "Particular Aspects of Periodontal Disease Pathogenesis." In Etiology and Pathogenesis of Periodontal Disease, 77–124. Berlin, Heidelberg: Springer Berlin Heidelberg, 2010. http://dx.doi.org/10.1007/978-3-642-03010-9_3.
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Dumitrescu, Alexandrina L. "Aspects of the Research Methodology for Periodontal Disease Assessment in Epidemiological Surveys." In Understanding Periodontal Research, 575–643. Berlin, Heidelberg: Springer Berlin Heidelberg, 2012. http://dx.doi.org/10.1007/978-3-642-28923-1_19.
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Goodeve, Anne. "von Willebrand Disease: Molecular Aspects." In Textbook of Hemophilia, 278–85. Oxford, UK: Wiley-Blackwell, 2010. http://dx.doi.org/10.1002/9781444318555.ch42.
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Hampshire, Daniel, and Anne Goodeve. "von Willebrand Disease: Molecular Aspects." In Textbook of Hemophilia, 353–61. Oxford, UK: John Wiley & Sons, Ltd, 2014. http://dx.doi.org/10.1002/9781118398258.ch48.
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Istace, Kathy. "More than just bad breath: periodontal disease." In An introduction to pet dental care: for veterinary nurses and technicians, 1–13. Wallingford: CABI, 2021. http://dx.doi.org/10.1079/9781789248869.0001.
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Kapetanaki, Maria G., Ana L. Mora, and Mauricio Rojas. "Aging Mesenchymal Stem Cells in Lung Disease." In Molecular Aspects of Aging, 159–71. Hoboken, NJ: John Wiley & Sons, Inc, 2014. http://dx.doi.org/10.1002/9781118396292.ch12.
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Boyer, Laurent, Jorge Boczkowski, and Serge Adnot. "COPD as a Disease of Premature Aging." In Molecular Aspects of Aging, 173–83. Hoboken, NJ: John Wiley & Sons, Inc, 2014. http://dx.doi.org/10.1002/9781118396292.ch13.
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Maslanka, Susan E. "Botulism as a Disease of Humans." In Molecular Aspects of Botulinum Neurotoxin, 259–89. New York, NY: Springer New York, 2014. http://dx.doi.org/10.1007/978-1-4614-9454-6_12.
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Balding, Elba, Katherine Ververis, and Tom C. Karagiannis. "Molecular Aspects of the Warburg Effect." In Molecular mechanisms and physiology of disease, 371–82. New York, NY: Springer New York, 2014. http://dx.doi.org/10.1007/978-1-4939-0706-9_13.
Pełny tekst źródłaStreszczenia konferencji na temat "Periodontal disease Molecular aspects"
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Stork, Larissa Rosa, Lucca Stephani Ribeiro, Izabella Savergnini Deprá, Luísa D’Ávila Camargo, and Maria Angélica Santos Novaes. "Tau protein and its role in Alzheimer’s disease physiopathology: a literature review." In XIII Congresso Paulista de Neurologia. Zeppelini Editorial e Comunicação, 2021. http://dx.doi.org/10.5327/1516-3180.132.
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Background: Alzheimer’s disease (AD) is a neurodegenerative disorder characterized by a double proteinopathy: deposition of amyloid-β into plaques and hyperphosphorylation of Tau protein. Objectives: To understand the genetic and molecular aspects of Tau protein and its relationship with Alzheimer’s disease. Methods: We conducted a systematic literature search using Pubmed/ MEDLINE and ClinicalKey databases, applying the descriptors: “Alzheimer Disease” AND “Tau proteins’’ AND Tauopathies, during July and August of 2020. The inclusion criteria were English and Portuguese articles published between 2015 and 2020, with human limited study and free full text, excluding images, books, clinical tests, and narrative reviews. After analyzing titles and abstracts, we selected 12 articles and included 7 additional studies. Results: Mapt, the encoder gene of Tau, is located in the 17q21.3 locus and presents 16 exons that, when transcripted, originates 12 copies of mRNA by alternative splicing and 6 Tau’s isoforms. Tau is a microtubule-associated protein (MAP) responsible for cellular cytoskeleton stabilization and maintenance, promoting neuronal axonal transport. A kinase-phosphatase imbalance turns Tau hyperphosphorylated, disassociating it from tubulin and grouping it into insoluble paired helical filaments, which originates neurofibrillary tangles. The tauopathy’s progress causes neurotransmitter destabilization and neuronal death, inducing AD symptomatic manifestations. Conclusions: Due to the gradual worsening of the disease to more debilitating stages, studies focused on deepening the knowledge of genetic and molecular aspects of Tau protein are viable and promising alternatives to improve the quality of patient’s lives.
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Sharma, Sonika, and Banshi D. Gupta. "Fiber Optic SPR based Dopamine Sensor utilizing GNP/SnO2 Nanocomposite Sup-ported Molecular Imprinting." In JSAP-OSA Joint Symposia. Washington, D.C.: Optica Publishing Group, 2017. http://dx.doi.org/10.1364/jsap.2017.6a_a410_6.
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Dopamine (DA) belongs to the catecholamine family of neurotransmitters and is very important for humans. It is produced in adrenal glands and several areas of the brain. Dopamine is formed by decarboxylation of DOPA and is a precursor of two other neurotransmitters adrenaline and noradrenalin. Dopamine is the most abundant of the catecholamine, hence affects many aspects of brain functionality such as movement, emotional response and ability to experience pain and pleasure. Dopamine also affects the cardiovascular and renal systems. Excessive secretion of DA (e.g., due to Huntington’s disease) is associated with failure in energy metabolism and causes untimely death. Differently low levels of dopamine in the central nervous system causes several neurological diseases, for example schizophrenia, Parkinson’s disease. Therefore, it is important to detect dopamine level efficiently in human body [1].
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Antonijević, Marko, Žiko Milanović, Edina Avdović, Dušica Simijonović, and Zoran Marković. "ANOTHER LOOK AT THE BIOLOGICAL ROLES OF A PLANT ALKALOID-BERBERINE." In XXVII savetovanje o biotehnologiji. University of Kragujevac, Faculty of Agronomy, 2022. http://dx.doi.org/10.46793/sbt27.455a.
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For millennia, berberine extracts or berberine itself has been the effective traditional drug with wide application due to its broad spectrum of antibiotic activity. A significant aspect of the berberine’s physiological activity that is often overlooked is the ability to go through the blood-brain barrier and has an impact on different processes and irregularities in the brain such as dementia and Alzheimer’s disease. Potential inhibitory activity towards enzymes for which is believed to be involved in these diseases, in this paper is confirmed by molecular docking simulations. Binding energies suggest that berberine exhibits good potential inhibitory activity and confirms that one of the aspects of suppression of Alzheimer’s disease and dementia is the inhibition of cholinesterase enzymes.
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De Luca, Amalia, Christina M. Warboys, Narges Amini, Pedro Ferreira, Peter Gatehouse, David Firmin, Justin Mason, Spencer Sherwin, and Paul C. Evans. "Image-Based Computational Hemodynamics and Microarray Analysis of the Porcine Aortic Arch Reveals a Correlation Between Shear Stress and Endothelial Cell Apoptosis." In ASME 2012 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2012. http://dx.doi.org/10.1115/sbc2012-80948.
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Atherosclerosis is a focal disease that occurs predominantly at regions of the arterial tree that are exposed to disturbed blood flow, which generates low, oscillatory wall shear stress (WSS) at the lumen. WSS controls the spatial distribution of lesions by influencing numerous aspects of endothelial cell (EC) physiology, including inflammatory activation and viability. Of particular note, ECs in low shear, lesion-prone regions are characterized by increased apoptosis and turnover rates1 thus providing a potential explanation for the distinct spatial localization of lesion formation. Although the molecular mechanisms underlying the effects of WSS on EC physiology are poorly understood, they are known to involve transcriptional changes.
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Hill, F. G. H., C. W. Williams, S. M. Enayat, and P. J. Darbyshire. "ASYMPTOMATIC vWD VARIANT WITH ABSENT RISTOCETIN ACTIVITY BUT PRESERVED BOTROCETIN ACTIVITY AND A DAUGHTER WITH TYPE III (HOMOZYGOUS) vWD." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1644109.
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The propositus, female aged 1 year, was investigated because of severe bruising. Bleeding time (BT) was in excess of 20 mins, VIIIC <0.01 u/ml and vWF Ag and ristocetin cofactor absent. Family studies showed:-Multimeric analysis was not possible on the propositus, but was normal in the plasma of all other family members. The father of the propositus, however, had an abnormal multimer pattern on lysed platelets, in that the faint low molecular weight doublet is absent and a dense band in the position of the lower band of the doublet with anodal and cathodal trailing.The maternal grandmother and mother appear to have asynpto-matic type I vWD and the father possibly has asymptomatic type I together with an alteration in the biologically vWF site with loss of the ristocetin site. This abnormality is not seen in his parents and his daughter possibly has type III vWD. The propositus' father although having some similarities to the patient of Howard et al., is different in other aspects.1. Howard MA, Salem HH. et al. (1982) Variant von Willebrand's disease Type B - Revisited. Blood, 60: 1420-1428.
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Santos, Alencar Pereira dos, Diogo Fernandes dos Santos, Isabela Maria Bernardes Goulart, Thales Junqueira Oliveira, Isabella Sabião Borges, Maria Fernanda Prado Rosa, Gabriel Nunes Melo Assunção, et al. "Early diagnosis of neural involvement in home contacts of leprosy patients: The experience of a national reference center between 2014- 2020." In XIII Congresso Paulista de Neurologia. Zeppelini Editorial e Comunicação, 2021. http://dx.doi.org/10.5327/1516-3180.605.
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Background: The long incubation period of leprosy, its insidious signs and symptoms produce difficulties in its diagnosis and correct clinical classification. The early recognition of neural impairment in leprosy, especially in household contacts with subclinical infection and in the primary neural form, in which the classic clinical and laboratory findings of the disease are, by definition, absent, represents a major challenge in clinical practice. Objectives: Characterize the clinical, molecular, serological and neurophysiological aspects in the early diagnosis of leprosy neuropathy, in household contacts with subclinical infection (positive ELISA anti-PGL1 serology. Design and setting: Longitudinal study carried out at the Clinics Hospital - Federal Univeristy of Uberlândia, a center specialized in Leprosy/Sanitary Dermatology. Methods: 361 seropositive household contacts (CDSP), defined as subclinical infection, were recruited, followed up at a national referral center for leprosy in Brazil, from 2014 to 2016. All individuals underwent a clinical, laboratory and neurophysiological evaluation. Results: 361 CDSP were evaluated. The qPCR analysis was positive in 35.5% (128/361) in the dermal shaving and in 25.8% (85/361) in the skin biopsy of the CDSP. In the electroneuromyographic evaluation, 23.5% (93/361) of the CDSP showed signs of neural involvement, with an average of 2.1 nerves compromised by CDSP. 62.3% (53/93) presented a pattern of mononeuropathy in ENMG. Conclusions: Annual monitoring of CDSP, a prevalence of peripheral neural impairment assessed by ENMG, favoring early treatment.
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Ferreira, Nancy, Darley Ferreira, and Thais Ferreira. "GENETIC EVALUATION OF MICROCALCIFICATIONS AS A PROGNOSTIC FACTOR." In Abstracts from the Brazilian Breast Cancer Symposium - BBCS 2021. Mastology, 2021. http://dx.doi.org/10.29289/259453942021v31s2101.
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Introduction: Breast cancer is the most recurring type of cancer among women, with reduced mortality at an initial stage of lesion. From a radiological perspective, perceived microcalcifications may be associated with histological findings such as proliferative injuries with or without atypical features and ductal carcinoma in situ. Currently, percutaneous and vacuum biopsies allow for the correlation between anatomoradiological and identification of previous lesions and those that offer the risk of cancer. No biomarker has been established to predict the risk of cancer in women diagnosed with benign mammary disease. Doing so could strengthen the possibility of stratifying the individual risk of benign injuries for cancer. The platelet-derived growth factor receptor A (PDGFRA) plays its part in tumor oncogenesis, angiogenesis, and metastasis, and its activation is found in some kinds of cancer. In contrast, DNA methylation standards are initial changes to the development of cancer and may be helpful in its early identification, being regulated by a family of enzymes called DNMTs (DNA methyltransferase). Methods: The aim of this study was to evaluate the profile of BI-RADS® 4 and 5 mammary microcalcification women carriers and determine the level of the gene expression of possible molecular markers in 37 patients with mammary microcalcification (paraffin blocks) and 26 patients with breast cancer (fresh in RNA later tissue) cared for at the Hospital Barão de Lucena’s Mastology Ambulatory. Anatomoradiological aspects along with clinical findings have been evaluated , and percentage rates have been calculated. The PDGFRA and DNMTs (DMNT3a) gene expressions have been established using quantitative polymerase chain reaction (qPCR), with the use of β-actin as reference gene. Discussion: In the patients with mammary microcalcification, the average age was 55.9; predominantly whiteskinned subjects (p<0.014). Most of them were mothers (p<0.001), and the average menarche age was 13. The subgroups that presented greater significance were patients classified BI-RADS® in category IV (67.6%) and histological findings of nonproliferative lesion (p<0.001). Lesions of the ductal carcinoma in situ type (100%) presented positive estrogen and progesterone receptors, and 94.6% have undergone sectorectomy surgery by prior needling (p<0.001). The most damaged breast was the left one (62.2%), and the most affected quadrant was the top lateral one (59.5%) (p<0.001). There was no family history in 83.8% of the cases. In the tested microcalcification samples, it was not possible to observe the expression of PDGFRA. Nevertheless, 15 out of 37 patients with microcalcification showed an increase in the gene expression of DMNT3a, most of them greater than Luminal and triple-negative cancer types. Conclusion: The data presented here highlight the improvement on the description of BI-RADS® 4 subclassification in order to better conduct the clinical decision and also demonstrated the potential of DNMTs evaluation in microcalcification samples as a strategy to access the understanding about the role of these molecules in the breast cancer development.
Raporty organizacyjne na temat "Periodontal disease Molecular aspects"
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Dawson, William O., Moshe Bar-Joseph, Charles L. Niblett, Ron Gafny, Richard F. Lee, and Munir Mawassi. Citrus Tristeza Virus: Molecular Approaches to Cross Protection. United States Department of Agriculture, January 1994. http://dx.doi.org/10.32747/1994.7570551.bard.
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Citrus tristeza virus (CTV) has the largest genomes among RNA viruses of plants. The 19,296-nt CTV genome codes for eleven open reading frames (ORFs) and can produce at least 19 protein products ranging in size from 6 to 401 kDa. The complex biology of CTV results in an unusual composition of CTV-specific RNAs in infected plants which includes multiple defective RNAs and mixed infections. The complex structure of CTV populations poses special problems for diagnosis, strain differentiation, and studies of pathogenesis. A manipulatable genetic system with the full-length cDNA copy of the CTV genome has been created which allows direct studies of various aspects of the CTV biology and pathology. This genetic system is being used to identify determinants of the decline and stem-pitting disease syndromes, as well as determinants responsible for aphid transmission.
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Shpigel, Nahum, Raul Barletta, Ilan Rosenshine, and Marcelo Chaffer. Identification and characterization of Mycobacterium paratuberculosis virulence genes expressed in vivo by negative selection. United States Department of Agriculture, January 2004. http://dx.doi.org/10.32747/2004.7696510.bard.
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Mycobacterium avium subsp. paratuberculosis (MAP) is the etiological agent of a severe inflammatory bowel disease (IBD) in ruminants, known as Johne’s disease or paratuberculosis. Johne’s disease is considered to be one of the most serious diseases affecting dairy cattle both in Israel and worldwide. Heavy economic losses are incurred by dairy farmers due to the severe effect of subclinical infection on milk production, fertility, lower disease resistance and early culling. Its influence in the United States alone is staggering, causing an estimated loss of $1.5 billion to the agriculture industry every year. Isolation of MAP from intestinal tissue and blood of Crohn's patients has lead to concern that it plays a potential pathogenic role in promoting human IDB including Crohn’s disease. There is great concern following the identification of the organism in animal products and shedding of the organism to the environment by subclinically infected animals. Little is known about the molecular basis for MAP virulence. The goal of the original proposed research was to identify MAP genes that are required for the critical stage of initial infection and colonization of ruminants’ intestine by MAP. We proposed to develop and use signature tag mutagenesis (STM) screen to find MAP genes that are specifically required for survival in ruminants upon experimental infection. This research projected was approved as one-year feasibility study to prove the ability of the research team to establish the animal model for mutant screening and alternative in-vitro cell systems. In Israel, neonatal goat kids were repeatedly inoculated with either one of the following organisms; MAP K-10 strain and three transposon mutants of K-10 which were produced and screened by the US PI. Six months after the commencement of inoculation we have necropsied the goats and taken multiple tissue samples from the jejunum, ileum and mesenteric lymph nodes. Both PCR and histopathology analysis indicated on efficient MAP colonization of all the inoculated animals. We have established several systems in the Israeli PI’s laboratory; these include using IS900 PCR for the identification of MAP and using HSP65-based PCR for the differentiation between MAV and MAP. We used Southern blot analysis for the differentiation among transposon mutants of K-10. In addition the Israeli PI has set up a panel of in-vitro screening systems for MAP mutants. These include assays to test adhesion, phagocytosis and survival of MAP to/within macrophages, assays that determine the rate of MAPinduced apoptosis of macrophages and MAP-induced NO production by macrophages, and assays testing the interference with T cell ã Interferon production and T cell proliferation by MAP infected macrophages (macrophage studies were done in BoMac and RAW cell lines, mouse peritoneal macrophages and bovine peripheral blood monocytes derived macrophages, respectively). All partners involved in this project feel that we are currently on track with this novel, highly challenging and ambitious research project. We have managed to establish the above described research systems that will clearly enable us to achieve the original proposed scientific objectives. We have proven ourselves as excellent collaborative groups with very high levels of complementary expertise. The Israeli groups were very fortunate to work with the US group and in a very short time period to master numerous techniques in the field of Mycobacterium research. The Israeli group has proven its ability to run this complicated animal model. This research, if continued, may elucidate new and basic aspects related to the pathogenesis MAP. In addition the work may identify new targets for vaccine and drug development. Considering the possibility that MAP might be a cause of human Crohn’s disease, better understanding of virulence mechanisms of this organism might also be of public health interest as well.
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Gottlieb, Yuval, Bradley Mullens, and Richard Stouthamer. investigation of the role of bacterial symbionts in regulating the biology and vector competence of Culicoides vectors of animal viruses. United States Department of Agriculture, June 2015. http://dx.doi.org/10.32747/2015.7699865.bard.
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Symbiotic bacteria have been shown to influence host reproduction and defense against biotic and abiotic stressors, and this relates to possible development of a symbiont-based control strategy. This project was based on the hypothesis that symbionts have a significant impact on Culicoides fitness and vector competence for animal viruses. The original objectives in our proposal were: 1. Molecular identification and localization of the newly-discovered symbiotic bacteria within C. imicola and C. schultzei in Israel and C. sonorensis in California. 2. Determination of the prevalence of symbiotic bacteria within different vector Culicoides populations. 3. Documentation of specific symbiont effects on vector reproduction and defense: 3a) test for cytoplasmic incompatibility in Cardinium-infected species; 3b) experimentally evaluate the role of the symbiont on infection or parasitism by key Culicoides natural enemies (iridescent virus and mermithid nematode). 4. Testing the role(s) of the symbionts in possible protection against infection of vector Culicoides by BTV. According to preliminary findings and difficulties in performing experimental procedures performed in other insect symbiosis systems where insect host cultures are easily maintained, we modified the last two objectives as follows: Obj. 3, we tested how symbionts affected general fitness of Israeli Culicoides species, and thoroughly described and evaluated the correlation between American Culicoides and their bacterial communities in the field. We also tried alternative methods to test symbiont-Culicoides interactions and launched studies to characterize low-temperature stress tolerances of the main US vector, which may be related to symbionts. Obj. 4, we tested the correlation between EHDV (instead of BTV) aquisition and Cardinium infection. Culicoides-bornearboviral diseases are emerging or re-emerging worldwide, causing direct and indirect economic losses as well as reduction in animal welfare. One novel strategy to reduce insects’ vectorial capacity is by manipulating specific symbionts to affect vector fitness or performance of the disease agent within. Little was known on the bacterial tenants occupying various Culicoides species, and thus, this project was initiated with the above aims. During this project, we were able to describe the symbiont Cardinium and whole bacterial communities in Israeli and American Culicoides species respectively. We showed that Cardinium infection prevalence is determined by land surface temperature, and this may be important to the larval stage. We also showed no patent significant effect of Cardinium on adult fitness parameters. We showed that the bacterial community in C. sonorensis varies significantly with the host’s developmental stage, but it varies little across multiple wastewater pond environments. This may indicate some specific biological interactions and allowed us to describe a “core microbiome” for C. sonorensis. The final set of analyses that include habitat sample is currently done, in order to separate the more intimately-associated bacteria from those inhabiting the gut contents or cuticle surface (which also could be important). We were also able to carefully study other biological aspects of Culicoides and were able to discriminate two species in C. schultzei group in Israel, and to investigate low temperature tolerances of C. sonorensis that may be related to symbionts. Scientific implications include the establishment of bacterial identification and interactions in Culicoides (our work is cited in other bacteria-Culicoides studies), the development molecular identification of C. schultzei group, and the detailed description of the microbiome of the immature and matched adult stages of C. sonorensis. Agricultural implications include understanding of intrinsic factors that govern Culicoides biology and population regulation, which may be relevant for vector control or reduction in pathogen transmission. Being able to precisely identify Culicoides species is central to understanding Culicoides borne disease epidemiology.
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Sessa, Guido, та Gregory Martin. MAP kinase cascades activated by SlMAPKKKε and their involvement in tomato resistance to bacterial pathogens. United States Department of Agriculture, січень 2012. http://dx.doi.org/10.32747/2012.7699834.bard.
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The research problem: Pseudomonas syringae pv. tomato (Pst) and Xanthomonas campestrispv. vesicatoria (Xcv) are the causal agents of tomato bacterial speck and spot diseases, respectively. These pathogens colonize the aerial parts of the plant and cause economically important losses to tomato yield worldwide. Control of speck and spot diseases by cultural practices or chemicals is not effective and genetic sources of resistance are very limited. In previous research supported by BARD, by gene expression profiling we identified signaling components involved in resistance to Xcvstrains. Follow up experiments revealed that a tomato gene encoding a MAP kinase kinase kinase (MAPKKKe) is required for resistance to Xcvand Pststrains. Goals: Central goal of this research was to investigate the molecular mechanisms by which MAPKKKεand associated MAP kinase cascades regulate host resistance. Specific objectives were to: 1. Determine whether MAPKKKεplays a broad role in defense signaling in plants; 2. Identify components of MAP kinase cascades acting downstream of MAPKKKε; 3. Determine the role of phosphorylation-related events in the function of MAPKKKε; 4. Isolate proteins directly activated by MAPKKKε-associatedMAPK modules. Our main achievements during this research program are in the following major areas: 1. Characterization of MAPKKKεas a positive regulator of cell death and dissection of downstream MAP kinase cascades (Melech-Bonfil et al., 2010; Melech-Bonfil and Sessa, 2011). The MAPKKKεgene was found to be required for tomato resistance to Xcvand Pstbacterial strains and for hypersensitive response cell death triggered by different R gene/effector gene pairs. In addition, overexpression analysis demonstrated that MAPKKKεis a positive regulator of cell death, whose activity depends on an intact kinase catalytic domain. Epistatic experiments delineated a signaling cascade downstream of MAPKKKεand identified SIPKK as a negative regulator of MAPKKKε-mediated cell death. Finally, genes encoding MAP kinase components downstream of MAPKKKεwere shown to contribute to tomato resistance to Xcv. 2. Identification of tomato proteins that interact with MAPKKKεand play a role in plant immunity (Oh et al., 2011). We identified proteins that interact with MAPKKKε. Among them, the 14-3-3 protein TFT7 was required for cell death mediated by several R proteins. In addition, TFT7 interacted with the MAPKK SlMKK2 and formed homodimersin vivo. Thus, TFT7 is proposed to recruit SlMKK2 and MAPKKK client proteins for efficient signal transfer. 3. Development of a chemical genetic approach to identify substrates of MAPKKKε-activated MAP kinase cascades (Salomon et al., 2009, 2011). This approach is based on engineering the kinase of interest to accept unnatural ATP analogs. For its implementation to identify substrates of MAPKKKε-activated MAP kinase modules, we sensitized the tomato MAP kinase SlMPK3 to ATP analogs and verified its ability to use them as phosphodonors. By using the sensitized SlMPK3 and radiolabeled N6(benzyl)ATP it should be possible to tag direct substrates of this kinase. 4. Development of methods to study immunity triggered by pathogen-associated molecular patterns (PAMPs) in tomato and N. benthamiana plants (Kim et al., 2009; Nguyen et al. 2010). We developed protocols for measuring various PTI-associatedphenotypes, including bacterial populations after pretreatment of leaves with PAMPs, induction of reporter genes, callose deposition at the cell wall, activation of MAP kinases, and a luciferase-based reporter system for use in protoplasts. Scientific and agricultural significance: Our research activities discovered and characterized a signal transduction pathway mediating plant immunity to bacterial pathogens. Increased understanding of molecular mechanisms of immunity will allow them to be manipulated by both molecular breeding and genetic engineering to produce plants with enhanced natural defense against disease. In addition, we successfully developed new biochemical and molecular methods that can be implemented in the study of plant immunity and other aspects of plant biology.
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Eldar, Avigdor, and Donald L. Evans. Streptococcus iniae Infections in Trout and Tilapia: Host-Pathogen Interactions, the Immune Response Toward the Pathogen and Vaccine Formulation. United States Department of Agriculture, December 2000. http://dx.doi.org/10.32747/2000.7575286.bard.
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In Israel and in the U.S., Streptococcus iniae is responsible for considerable losses in various fish species. Poor understanding of its virulence factors and limited know-how-to of vaccine formulation and administration are the main reasons for the limited efficacy of vaccines. Our strategy was that in order to Improve control measures, both aspects should be equally addressed. Our proposal included the following objectives: (i) construction of host-pathogen interaction models; (ii) characterization of virulence factors and immunodominant antigens, with assessment of their relative importance in terms of protection and (iii) genetic identification of virulence factors and genes, with evaluation of the protective effect of recombinant proteins. We have shown that two different serotypes are involved. Their capsular polysaccharides (CPS) were characterized, and proved to play an important role in immune evasion and in other consequences of the infection. This is an innovative finding in fish bacteriology and resembles what, in other fields, has become apparent in the recent years: S. iniae alters surface antigens. By so doing, the pathogen escapes immune destruction. Immunological assays (agar-gel immunodiffusion and antibody titers) confirmed that only limited cross recognition between the two types occurs and that capsular polysaccharides are immunodominant. Vaccination with purified CPS (as an acellular vaccine) results in protection. In vitro and ex-vivo models have allowed us to unravel additional insights of the host-pathogen interactions. S. iniae 173 (type II) produced DNA fragmentation of TMB-8 cells characteristic of cellular necrosis; the same isolate also prevented the development of apoptosis in NCC. This was determined by finding reduced expression of phosphotidylserine (PS) on the outer membrane leaflet of NCC. NCC treated with this isolate had very high levels of cellular necrosis compared to all other isolates. This cellular pathology was confirmed by observing reduced DNA laddering in these same treated cells. Transmission EM also showed characteristic necrotic cellular changes in treated cells. To determine if the (in vitro) PCD/apoptosis protective effects of #173 correlated with any in vivo activity, tilapia were injected IV with #173 and #164 (an Israeli type I strain). Following injection, purified NCC were tested (in vitro) for cytotoxicity against HL-60 target cells. Four significant observations were made : (i) fish injected with #173 had 100-400% increased cytotoxicity compared to #164 (ii) in vivo activation occurred within 5 minutes of injection; (iii) activation occurred only within the peripheral blood compartment; and (iv) the isolate that protected NCC from apoptosis in vitro caused in vivo activation of cytotoxicity. The levels of in vivo cytotoxicity responses are associated with certain pathogens (pathogen associated molecular patterns/PAMP) and with the tissue of origin of NCC. NCC from different tissue (i.e. PBL, anterior kidney, spleen) exist in different states of differentiation. Random amplified polymorphic DNA (RAPD) analysis revealed the "adaptation" of the bacterium to the vaccinated environment, suggesting a "Darwinian-like" evolution of any bacterium. Due to the selective pressure which has occurred in the vaccinated environment, type II strains, able to evade the protective response elicited by the vaccine, have evolved from type I strains. The increased virulence through the appropriation of a novel antigenic composition conforms with pathogenic mechanisms described for other streptococci. Vaccine efficacy was improved: water-in-oil formulations were found effective in inducing protection that lasted for a period of (at least) 6 months. Protection was evaluated by functional tests - the protective effect, and immunological parameters - elicitation of T- and B-cells proliferation. Vaccinated fish were found to be resistant to the disease for (at least) six months; protection was accompanied by activation of the cellular and the humoral branches.