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Search Results: 1 - 10 of 44881 matches for " Michael Centola "
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Steroid-refractory ulcerative colitis treated with corticosteroids, metronidazole and vancomycin: a case report
Jonathan Miner, M Monem Gillan, Philip Alex, Michael Centola
BMC Gastroenterology , 2005, DOI: 10.1186/1471-230x-5-3
Abstract: We report a provocative case of UC with profound rheumatologic involvement directly preceded by Clostridium difficile infection and accompanying fever, vomiting, bloody diarrhea, and arthritis. Colonic biopsy revealed a histopathology suggestive of UC. Antibiotic treatment eliminated detectable levels of enteric pathogens but did not abate symptoms. Resolution of symptoms was procurable with oral prednisone, but tapering of corticosteroids was only achievable in combination therapy with vancomycin and metronidazole.An infectious pathogen may have both precipitated and exacerbated autoimmune disease attributes in UC, symptoms of which could be resolved only with a combination of corticosteroids, vancomycin and metronidazole. This may warrant the need for more perceptive scrutiny of C. difficile and the like in patients with UC.Clostridium difficile infection may be a compounding factor in ulcerative colitis (UC) with data suggestive of a role in disease exacerbation or initiation by the organism in a subset of patients [1]. Adjunctive antibiotic therapy, either broad-spectrum or gram positive-specific, has shown limited efficacy in UC [2,3]. However, sporadic reports in which significant therapeutic potential was achieved [4-6] suggest that a distinct subclass of patients with an infectious-associated phenotype may exist. Although there have been an increasing number of case reports on ulcerative colitis complicated by cytomegalovirus infection [7-9], there are few with conclusive evidence of infection with Clostridium difficile. Herein, we report a case of steroid-resistant UC with profound rheumatologic involvement immediately preceded by C. difficile infection in which remission of UC symptoms was twice achieved in response to adjunct metronidazole and vancomycin therapy. The patient remained symptom-free without supportive therapy for a four-year period.A 32-year-old white male presented with nausea, vomiting, crampy lower abdominal pain and diarrhea. His initial
Neutrophils: the forgotten cell in JIA disease pathogenesis
James N Jarvis, Kaiyu Jiang, Howard R Petty, Michael Centola
Pediatric Rheumatology , 2007, DOI: 10.1186/1546-0096-5-13
Abstract: The nomenclature used to categorize children with chronic arthritis has undergone considerable change over the years covered by this review. The most widely accepted classification scheme replaces the terms juvenile rheumatoid arthritis and juvenile chronic arthritis with the term juvenile idiopathic arthritis. However, it is important for the reader to note that the terms are not synonymous and classification schemes do not completely overlap. This leaves the reviewer with the vexing task of how to refer to earlier studies that used different classification schemes. For the sake of simplicity, clarity, and accuracy, we have elected to use whatever terms were used by the authors of the relevant studies in describing those studies, while adhering to the internationally-accepted classification scheme when speaking generically of chronic arthritis in children.With the possible exception of the systemic-onset form [1], juvenile idiopathic arthritis (JIA) has long been assumed to be an "autoimmune" disease. The autoimmune theory of pathogenesis has tenaciously held its position of unchallenged dogma in pediatric rheumatology, despite serious limits in its ability to explain all the known immunopathological phenomena and the paucity of evidence for either a T- or B-cell driven response (see below). At the same time, no competing theories for pathogenesis have emerged, so the autoimmune theory holds its ground by default. In this review, we will discuss emerging evidence that demonstrates the importance of neutrophils in regulating and informing the adaptive immune response, suggesting, therefore, that innate immunity may play a larger role in JIA pathogenesis than has been previously thought. We will then summarize new data from our laboratories that supports the hypothesis that neutrophil activation in JIA is a primary pathogenic event, and that involvement of the adaptive immune system is downstream of that primary event.This paper is not intended as a comprehensive rev
Statistical monitoring of weak spots for improvement of normalization and ratio estimates in microarrays
Igor Dozmorov, Nicholas Knowlton, Yuhong Tang, Michael Centola
BMC Bioinformatics , 2004, DOI: 10.1186/1471-2105-5-53
Abstract: We developed a multistep procedure for analysis of mRNA expression data that robustly identifies the additive noise in a microarray experiment. This analysis is predicated on the fact that additive noise signals can be accurately identified by both distribution and statistical analysis.Identification of additive noise in this manner allows exclusion of noncorrelated weak signals from regression-based normalization of compared profiles thus maximizing the accuracy of these methods. Moreover, genes expressed at very low levels can be clearly identified due to the fact that their expression distribution is stable and distinguishable from the random pattern of additive noise.Microarrays are powerful and cost-effective tools for large-scale analysis of gene expression. While the utility of this technology has been established [1,2], analytical methods are evolving and a matter of contention. Key among the more controversial aspects is the treatment of data from weak spots, which significantly influences outcomes. For example, ratio analysis is commonly employed to determine expression differences between two samples. However any procedure that uses raw intensities to infer relative expression is limited due to the fact that accuracy is signal level dependent, with variation increasing dramatically for low intensity signals [1,3]. Several methods have been developed to diminish the influence of additive noise. One solution is to ignore any genes whose transcripts are present at a low total abundance, to exclude weak spots – arbitrarily (in Kooperberg etal., [3] an intensity cutoff was used such that the relative error in ratios was less than 25%) or with some statistical procedures [4,5]. Other methods proposed for discriminating expressed genes from those not expressed, such as the method of Greller and Tobin [6], are suitable only for bimodal distributions in which the distribution of intensities for these two subsets are non-overlapping, unlike many empirical data sets
Cascade Dynamics of Multiplex Propagation
Damon Centola,Michael W. Macy,Victor M. Eguiluz
Physics , 2005, DOI: 10.1016/j.physa.2006.06.018
Abstract: Random links between otherwise distant nodes can greatly facilitate the propagation of disease or information, provided contagion can be transmitted by a single active node. However we show that when the propagation requires simultaneous exposure to multiple sources of activation, called multiplex propagation, the effect of random links is just the opposite: it makes the propagation more difficult to achieve. We calculate analytical and numerically critical points for a threshold model in several classes of complex networks, including an empirical social network.
Failure in Complex Social Networks
Damon Centola
Physics , 2007,
Abstract: Tolerance against failures and errors is an important feature of many complex networked systems [1,2]. It has been shown that a class of inhomogeneously wired networks called scale-free[1,3] networks can be surprisingly robust to failures, suggesting that socially self-organized systems such as the World-Wide Web, the Internet, and other kinds of social networks [4] may have significant tolerance against failures by virtue of their scale-free degree distribution. I show that this finding only holds on the assumption that the diffusion process supported by the network is a simple one, requiring only a single contact in order for transmission to be successful.
Novel approaches to gene expression analysis of active polyarticular juvenile rheumatoid arthritis
James N Jarvis, Igor Dozmorov, Kaiyu Jiang, Mark Frank, Peter Szodoray, Philip Alex, Michael Centola
Arthritis Research & Therapy , 2004, DOI: 10.1186/ar1018
Abstract: 'Juvenile rheumatoid arthritis' (JRA), a term for the most prevalent form of arthritis in children, is applied to a family of illnesses characterized by chronic inflammation and hypertrophy of the synovial membranes. The term overlaps, but is not completely synonymous, with the family of illnesses referred to as juvenile chronic arthritis and/or juvenile idiopathic arthritis in Europe. We [1] and others [2] have proposed that the pathogenesis of rheumatoid disease in adults and children involves complex interactions between innate and adaptive immunity. This complexity lies at the core of the difficulty of unraveling disease pathogenesis. Both innate and adaptive immune systems use multiple cell types, a vast array of cell-surface and secreted proteins, and interconnected networks of positive and negative feedback [3]. Furthermore, while separable in thought, the innate and adaptive wings of the immune system are functionally intersected [4], and pathologic events occurring at these intersecting points are likely to be highly relevant to our understanding of pathogenesis of adult and childhood forms of chronic arthritis [5].Polyarticular JRA is a distinct clinical subtype characterized by inflammation and synovial proliferation in multiple joints (four or more), including the small joints of the hands [6]. This subtype of JRA may be severe, because of both its multiple joint involvement and its capacity to progress rapidly over time. Although clinically distinct, polyarticular JRA is not homogeneous, and patients vary in disease manifestations, age of onset, prognosis, and therapeutic response. These differences very likely reflect a spectrum of variation in the nature of the immune and inflammatory attack that can occur in this disease [1].Gene expression profiling using microarrays provides a highly parallel assay for assessing molecular pathophysiology in a comprehensive manner. It holds the potential to refine our understanding of complex disease states. However
Temporal dynamics of gene expression in the lung in a baboon model of E. coli sepsis
Hua Zhu, Yuhong Tang, Lacramioara Ivanciu, Michael Centola, Cristina Lupu, Fletcher B Taylor, Florea Lupu
BMC Genomics , 2007, DOI: 10.1186/1471-2164-8-58
Abstract: Using human oligonucleotide microarrays, we have explored the temporal changes of gene expression in the lung of baboons challenged with sublethal doses of E. coli. Temporal expression pattern and biological significance of the differentially expressed genes were explored using clustering and pathway analysis software. Expression of selected genes was validated by real-time PCR. Cytokine levels in tissue and plasma were assayed by multiplex ELISA. Changes in lung ultrastructure were visualized by electron microscopy. We found that genes involved in primary inflammation, innate immune response, and apoptosis peaked at 2 hrs. Inflammatory and immune response genes that function in the stimulation of monocytes, natural killer and T-cells, and in the modulation of cell adhesion peaked at 8 hrs, while genes involved in wound healing and functional recovery were upregulated at 24 hrs.The analysis of gene expression modulation in response to sepsis provides the baseline information that is crucial for the understanding of the pathophysiology of systemic inflammation and may facilitate the development of future approaches for sepsis therapy.Sepsis and its complications represent a complex disease encompassing multiple pathological processes, including uncontrolled systemic inflammation, coagulopathy, microvascular and hemodynamic abnormalities. The development of septic shock, acute respiratory distress syndrome (ARDS) and the onset of multiple organ (lung, liver, kidney, heart) dysfunction (MOD) are landmarks of severe sepsis, one of the leading causes of mortality in critically ill patients[1]. Despite significant progress, the pathophysiology of sepsis and its sequels are still not fully understood. One early MOD symptom associated with sepsis is acute lung injury[2]. Lipopolysaccharide (LPS) was considered the main component in the induction of lung injury in gram-negative bacterial sepsis. LPS recognition by host's Toll-Like Receptors (TLRs) is followed by subsequent a
Analysis of the interaction of extracellular matrix and phenotype of bladder cancer cells
Mikhail G Dozmorov, Kimberly D Kyker, Ricardo Saban, Nicholas Knowlton, Igor Dozmorov, Michael B Centola, Robert E Hurst
BMC Cancer , 2006, DOI: 10.1186/1471-2407-6-12
Abstract: Five bladder cancer cell lines and one immortalized, but non-tumorigenic, urothelial line were grown on Matrigel, a cancer-derived ECM, on SISgel, a normal-derived ECM, and on plastic, where the only ECM is derived from the cells themselves. The transcriptomes were analyzed on an array of 1186 well-annotated cancer derived cDNAs containing most of the major pathways for malignancy. Hypervariable genes expressing more variability across cell lines than a set expressing technical variability were analyzed further. Expression values were clustered, and to identify genes most likely to represent biological factors, statistically over-represented ontologies and transcriptional regulatory elements were identified.Approximately 400 of the 1186 total genes were expressed 2 SD above background. Approximately 100 genes were hypervariable in cells grown on each ECM, but the pattern was different in each case. A core of 20 were identified as hypervariable under all 3 growth conditions, and 33 were hypervariable on both SISgel and Matrigel, but not on plastic. Clustering of the hypervariable genes showed very different patterns for the same 6 cell types on the different ECM. Even when loss of cell cycle regulation was identified, different genes were involved, depending on the ECM. Under the most permissive conditions of growth where the malignant phenotype was fully expressed, activation of AKT was noted. TGFβ1 signaling played a major role in the response of bladder cancer cells to ECM. Identification of TREs on genes that clustered together suggested some clustering was driven by specific transcription factors.The extracellular matrix on which cancer cells are grown has a major effect on gene expression. A core of 20 malignancy-related genes were not affected by matrix, and 33 were differentially expressed on 3-dimensional culture as opposed to plastic. Other than these genes, the patterns of expression were very different in cells grown on SISgel than on Matrigel or even pla
Discriminators of mouse bladder response to intravesical Bacillus Calmette-Guerin (BCG)
Marcia R Saban, Cindy Simpson, Carole Davis, Gemma Wallis, Nicholas Knowlton, Mark Frank, Michael Centola, Randle M Gallucci, Ricardo Saban
BMC Immunology , 2007, DOI: 10.1186/1471-2172-8-6
Abstract: C57BL/6 female mice received four weekly instillations of BCG, LPS, or TNF-α. Morphometric analyses were conducted in bladders isolated from all groups and urine was collected for multiplex analysis of 18 cytokines. In addition, chromatin immune precipitation combined with real-time polymerase chain reaction assay (CHIP/Q-PCR) was used to test whether intravesical BCG would alter bladder cytokine gene expression.Acute BCG instillation induced edema which was progressively replaced by an inflammatory infiltrate, composed primarily of neutrophils, in response to weekly administrations. Our morphological analysis suggests that these polymorphonuclear neutrophils are of prime importance for the bladder responses to BCG. Overall, the inflammation induced by BCG was higher than LPS or TNF-α treatment but the major difference observed was the unique granuloma formation in response to BCG. Among the cytokines measured, this study highlighted the importance of IL-1β, IL-2, IL-3, IL-4, IL-6, IL-10, IL-17, GM-CSF, KC, and Rantes as discriminators between generalized inflammation and BCG-specific inflammatory responses. CHIP/Q-PCR indicates that acute BCG instillation induced an up-regulation of IL-17A, IL-17B, and IL-17RA, whereas chronic BCG induced IL-17B, IL-17RA, and IL-17RB.To the best of our knowledge, the present work is the first to report that BCG induces an increase in the IL-17 family genes. In addition, BCG induces a unique type of persisting bladder inflammation different from TNF-α, LPS, and, most likely, other classical pro-inflammatory stimuli.Intravesical Bacillus Calmette-Guerin (BCG) has been presented as a promising option for treatment of interstitial cystitis [1]. However, intravesical BCG is best known as the most effective agent for the treatment of high-grade superficial bladder cancer [2-4]. In this context, BCG is used to reduce both the recurrence rate of bladder tumor and to diminish the risk of its progression [2,3]. As an adjunct to transurethral
The Spontaneous Emergence of Conventions: An Experimental Study of Cultural Evolution
Damon Centola,Andrea Baronchelli
Computer Science , 2015, DOI: 10.1073/pnas.1418838112
Abstract: How do shared conventions emerge in complex decentralized social systems? This question engages fields as diverse as linguistics, sociology and cognitive science. Previous empirical attempts to solve this puzzle all presuppose that formal or informal institutions, such as incentives for global agreement, coordinated leadership, or aggregated information about the population, are needed to facilitate a solution. Evolutionary theories of social conventions, by contrast, hypothesize that such institutions are not necessary in order for social conventions to form. However, empirical tests of this hypothesis have been hindered by the difficulties of evaluating the real-time creation of new collective behaviors in large decentralized populations. Here, we present experimental results - replicated at several scales - that demonstrate the spontaneous creation of universally adopted social conventions, and show how simple changes in a population's network structure can direct the dynamics of norm formation, driving human populations with no ambition for large scale coordination to rapidly evolve shared social conventions.
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