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RHEUMATOLOGY (76 journals)

Showing 1 - 76 of 76 Journals sorted alphabetically
ACR Open Rheumatology     Open Access   (Followers: 6)
Advances in Rheumatology     Open Access   (Followers: 3)
African Journal of Rheumatology     Full-text available via subscription  
Aktuelle Rheumatologie     Hybrid Journal   (Followers: 2)
Annals of Rheumatology and Autoimmunity     Open Access   (Followers: 3)
Annals of the Rheumatic Diseases     Hybrid Journal   (Followers: 34)
Archives of Osteoporosis     Hybrid Journal   (Followers: 1)
Arthritis & Rheumatology     Hybrid Journal   (Followers: 65)
Arthritis Care & Research     Hybrid Journal   (Followers: 37)
Arthritis Research & Therapy     Open Access   (Followers: 14)
Australasian Musculoskeletal Medicine     Full-text available via subscription   (Followers: 5)
Best Practice & Research Clinical Rheumatology     Hybrid Journal   (Followers: 17)
BMC Musculoskeletal Disorders     Open Access   (Followers: 29)
BMC Rheumatology     Open Access   (Followers: 5)
Case Reports in Rheumatology     Open Access   (Followers: 10)
Clinical and Experimental Rheumatology     Full-text available via subscription   (Followers: 3)
Clinical Medicine Insights : Arthritis and Musculoskeletal Disorders     Open Access   (Followers: 3)
Clinical Rheumatology     Hybrid Journal   (Followers: 22)
Current Opinion in Rheumatology     Hybrid Journal   (Followers: 13)
Current Reviews in Musculoskeletal Medicine     Open Access   (Followers: 13)
Current Rheumatology Reports     Hybrid Journal   (Followers: 3)
Current Rheumatology Reviews     Hybrid Journal   (Followers: 4)
Current Treatment Options in Rheumatology     Hybrid Journal  
Egyptian Rheumatologist     Open Access   (Followers: 1)
Egyptian Rheumatology and Rehabilitation     Open Access   (Followers: 2)
Forum Reumatologiczne     Hybrid Journal  
Future Rheumatology     Full-text available via subscription   (Followers: 1)
Gait & Posture     Hybrid Journal   (Followers: 17)
Indian Journal of Rheumatology     Open Access   (Followers: 1)
Indonesian Journal of Rheumatology     Open Access  
International Journal of Clinical Rheumatology     Open Access   (Followers: 5)
International Journal of Rheumatic Diseases     Hybrid Journal   (Followers: 2)
International Journal of Rheumatology     Open Access   (Followers: 6)
International Musculoskeletal Medicine     Hybrid Journal   (Followers: 7)
Internet Journal of Rheumatology and Clinical Immunology     Open Access   (Followers: 4)
JCR Journal of Clinical Rheumatology     Hybrid Journal   (Followers: 7)
Journal of Musculoskeletal Research     Hybrid Journal   (Followers: 9)
Journal of Orthopedics & Rheumatology     Open Access  
Journal of Rheumatology     Open Access   (Followers: 32)
Modern Rheumatology     Hybrid Journal   (Followers: 4)
Modern Rheumatology Case Reports     Hybrid Journal  
Multiple Sclerosis and Related Disorders     Hybrid Journal   (Followers: 8)
Musculoskeletal Care     Hybrid Journal   (Followers: 19)
MYOPAIN. A journal of myofascial pain and fibromyalgia     Hybrid Journal   (Followers: 16)
Nature Reviews Rheumatology     Full-text available via subscription   (Followers: 25)
OA Arthritis     Open Access   (Followers: 1)
OA Inflammation     Open Access  
Open Access Rheumatology: Research and Reviews     Open Access   (Followers: 3)
Open Journal of Orthopedics and Rheumatology     Open Access  
Open Journal of Rheumatology and Autoimmune Diseases     Open Access   (Followers: 4)
Open Rheumatology Journal     Open Access  
Orthopädie & Rheuma     Full-text available via subscription  
Osteoarthritis and Cartilage     Full-text available via subscription   (Followers: 20)
Osteoarthritis and Cartilage Open     Open Access  
Osteologie     Hybrid Journal  
Osteoporosis and Sarcopenia     Open Access  
Pain. Joints. Spine     Open Access   (Followers: 1)
Reumatismo     Open Access  
Reumatología Clínica (English Edition)     Full-text available via subscription  
Revista Argentina de Reumatología     Open Access  
Revista Colombiana de Reumatologia     Open Access  
Revista Colombiana de Reumatología (English Edition)     Hybrid Journal  
rheuma plus     Hybrid Journal  
Rheumatic Disease Clinics of North America     Full-text available via subscription   (Followers: 4)
Rheumatica Acta: Open Access     Open Access  
Rheumatology     Hybrid Journal   (Followers: 34)
Rheumatology & Autoimmunity     Open Access   (Followers: 9)
Rheumatology Advances in Practice     Open Access   (Followers: 1)
Rheumatology and Therapy     Open Access   (Followers: 3)
Rheumatology International     Hybrid Journal   (Followers: 3)
Rheumatology Practice and Research     Open Access  
RMD Open     Open Access   (Followers: 1)
Scandinavian Journal of Rheumatology     Hybrid Journal   (Followers: 5)
Seminars in Arthritis and Rheumatism     Hybrid Journal   (Followers: 8)
The Lancet Rheumatology     Hybrid Journal   (Followers: 1)
Zeitschrift fur Rheumatologie     Hybrid Journal   (Followers: 6)
Similar Journals
Journal Cover
OA Inflammation
Number of Followers: 0  

  This is an Open Access Journal Open Access journal
ISSN (Online) 2052-787X
Published by OA Publishing London Homepage  [37 journals]
  • Cross-talk between vitamin D, estrogen and corticosteroids in
           glucocorticoid resistant asthma.

    • Abstract: Glucocorticoids (GC) are mainstay of therapy in asthma but over 50% of asthmatics do not respond to inhaled or oral glucocorticoids. This makes glucocorticoid resistance in asthma a challenging healthcare problem associated with significant morbidityand life-threatening disease progression. Physiologic and pharmacologic actions of glucocorticoids are mediated through binding to their receptors. Interaction of GC with glucocorticoid response elements regulates transcription of anti-inflammatory genes. Glucocorticoid actions are affected by post-translational modification of glucocorticoid receptor (GR), alterations in GR levels, or by actions that counteract its effects on downstream targets. Interplay between sex steroids and secosteroids such as vitamin D, has been shown to alter anti-inflammatory action of glucocorticoids. Given the structural similarities of steroid hormone molecules and their receptors, their co-localization in cells, and similar mechanisms on gene regulation and signaling, it is possible that cross talk between these molecules affects GC function and GC resistance.  In patients with steroid resistant asthma, there appear to be defectsin GCinduced gene transcription of anti-inflammatory mediatorssuch as IL10 and mitogen-activated protein kinase phosphatase-1 (MKP-1). Presence of vitamin D may reverse this defectby enhancing GC mediated transcription of genes of IL10 and MKP-1.Anti-inflammatory actions of glucocorticoids may differ by gender. In women asthma may be less responsive to corticosteroid treatment, as estrogen alters GR levelsthrough protein degradation and suppression of GC mediated transcription of anti-inflammatory proteins, such as MKP1 and glucocorticoid-induced leucine zipper protein (GLIZ). We discuss mechanism of glucocorticoid actions and how estrogen and vitamin D may affect its function and resistance.
      PubDate: 09/06/2014 07:20:43 am
       
  • NF-kB as a crucial factor for intracranial aneurysm formation and the
           potential of statins as drugs for intracranial aneurysm treatment through
           their anti-NF-kB effect.

    • Abstract: The article has been forwarded to the production team. The processing may take few weeks. Then the proof will be forwarded to the corresponding author. The final PDF and HTML files will be uploaded when the corrections to the proof are returned by the corresponding author.
      PubDate: 07/28/2014 04:31:02 pm
       
  • Role of epidermal growth factor receptor transactivation in the
           amplification of Helicobacter pylori-elicited induction in gastric mucosal
           expression of cyclooxygenase-2 and inducible nitric oxide synthase.

    • Abstract:   Introduction Invasion of gastric mucosa by Helicobacter pylori triggers a pattern of inflammatory responses initiated by the activation of mitogen-activated protein kinase (MAPK) cascade, resulting in the induction in cyclooxygenase-2 (COX-2) and inducible nitric oxide synthase (iNOS) and the excessive generation of prostaglandin (PGE2) and nitric oxide (NO). In this study, we report on the role of epidermal growth factor receptor (EGFR) transactivation in H. pylori lipopolysaccharide (LPS)-elicited induction in gastric mucosal expression of COX-2 and iNOS. We show that EGFR transactivation by H. pylori LPS occurs with the involvement of p38 MAPK and matrix metalloproteinase (MMP) activation and does not require Src kinase participation. Conclusion EGFR transactivation results in the amplification of the LPS-induced ERK phosphorylation and up-regulation in ERK-mediated IKK-β activation for the enhanced induction of NF-κB-dependent expression of iNOS. The rise in iNOS-dependent NO generation, in turn, leads to an up-regulation in COX-2 activation through S-nitrosylation and excessive PGE2 production. Taken together, our data provide strong indications of the involvement of EGFR transactivation in the amplification of ERK signalling cascade associated with up-regulation in gastric mucosal induction of iNOS and COX-2, and excessive NO and PGE2 generation in response to H. pylori.
      PubDate: 04/15/2014 12:15:02 pm
       
  • Hydrogen sulphide, systemic inflammatory response syndrome and
           compensatory anti-inflammatory response syndrome following sepsis.

    • Abstract:   Introduction Polymicrobial sepsis (PMS) is a systemic infection, which results in a highly evolved inflammatory response by the body; this response is ideally controlled by a signalled anti-inflammatory response. However, tissue damage and infection can cause these responses to become unregulated and pathological. Initially, a hyperimmune response can cause clotting and result in high levels of reactive oxygen species and inflammatory cytokines; when unregulated, this can result in multiple organ failure and death. Conversely, the anti-inflammatory response can become unregulated and result in immune paralysis, uncontrolled infection and pathological hypothermia. The novel signalling molecule hydrogen sulphide appears to be involved in immune function following sepsis. Several studies show that inhibiting the endogenous production of hydrogen sulphide is beneficial following sepsis, and administration of hydrogen sulphide donors appears to exacerbate sepsis. Some studies appear to show the opposite effect. In this review, we argue that these discrepancies could be due to the animal model used that resulted in a hyper- or hypoimmune response in conjunction with differing effects of hydrogen sulphide depending on its concentration and source. Conclusion PMS results in two responses by the body, systemic inflammatory response syndrome (SIRS) and compensatory anti-inflammatory response syndrome (CARS). The body produces hydrogen sulphide, and manipulation of it can be therapeutic to SIRS and CARS. Further studies on animal models need to be done to get a greater understanding of the role of hydrogen sulphide in SIRS and CARS, so that such knowledge can then be translated to the clinic.
      PubDate: 04/15/2014 12:15:02 pm
       
  • Post-transcriptional regulation of tumour necrosis factor alpha
           biosynthesis: Relevance to the pathophysiology of rheumatoid arthritis.

    • Abstract:   Introduction Expressed in response to injury or infection, tumour necrosis factor-alpha (TNF-α ) is a highly potent mediator of inflammation. Controlled expression of TNF-α is crucial, since overexpression can lead to autoimmune disease and tissue damage. TNF-α expression is regulated at different levels, including transcription, mRNA turnover and translation. Many reviews have focused on the signalling pathways that mediate cellular responses following TNF-α receptor engagement. In this article, we focus on an aspect that shows promise for pharmaceutical intervention, namely intracellular mechanisms regulating production of TNF-α in immune cells, especially post-transcriptional checkpoints. We discuss the roles of adenosine-uridine-rich-element-binding proteins, micro-RNA and MAP kinase in the post-transcriptional regulation of TNF-α mRNA activity and their relevance to the physiopathology of rheumatoid arthritis. Conclusion: A better understanding of the intracellular proteins and signalling pathways that regulate TNF-α biosynthesis is crucial to the development of novel anti-TNF-based therapies for rheumatoid arthritis patients.
      PubDate: 04/15/2014 12:15:02 pm
       
  • Tyrphostins as a promising therapeutic tool in inflammation-related
           conditions.

    • Abstract: Introduction Protein kinases regulate the expression of many genes that are pivotal for inflammation. This review aims to summarize data on a group of small molecules capable to inhibit tyrosine kinases, named tyrphostins. They are derivatives of benzylidene malonitrile thatdecrease tyrosine phosphorilation, thereby affecting not a single mediator, but cell signaling transduction. No single animal model fully represents the human disease, but the models therefore provide valuable tools to understand particular pathways. Here, we describe some of the recent investigations on tyrphostins as anti-inflammatory agents in vivo in animal models, and in vitro in cell culture systems. Conclusion It is anticipated that that this class of compounds is suitable for the treatment of inflammation-related diseases. Future research is required to understand the mechanisms of their action to pave way for gaining pharmacological benefits in clinical practice.
      PubDate: 04/15/2014 12:15:02 pm
       
  • Anti-hepatic fibrosis effects of traditional Chinese medicine: A review.

    • Abstract: Introduction Hepatic fibrosis (HF) is characterized by excessive deposition of extracellular matrix (ECM) proteins, such as collagen types I, III, IV and V, laminin and elastin, which leads to severe pathophysiological disturbances: remodeling of liver architecture, development of intrahepatic shunts, liver insufficiency, portal hypertension, esophageal varices, ascites and encephalopathic coma. In spite of the high incidence of HF worldwide, no generally accepted anti-fibrogenic therapy is available. At present, many researches about the anti-hepatic fibrosis drug are focus on the traditional Chinese medicines (TCM), which have been used in China for thousands of years and now are being manufactured in China, in standardized form in terms of quality and quantities of ingredients. Conclusion In a prospective study, many traditional Chinese medicines were found to play a chemopreventive role in the development of HF. And several laboratories, including ours, have clearly demonstrated the preventive and therapeutic effects of some Chinese herbal medicines on experimental HF, which may provide valuable information on the search for novel anti-fibrogenic agent.
      PubDate: 04/15/2014 12:15:02 pm
       
  • Vitamin D level and potential impact on immune cells in Behçet’s
           disease.

    • Abstract: Vitamin D plays key roles in innate and adaptive immunity through the stimulation of Toll-like receptors, increasing pro-inflammatory cytokine production, and possibly skewing T helper (Th) responses. Data from human vitamin D supplementation studies have shown beneficial effects of vitamin D on immune function, in particular in the context of autoimmunity. Low levels of this hormone were observed in several autoimmune diseases including Behçet disease (BD). The data relating vitamin D to autoimmune and inflammatory diseases are equivocal with studies linking low vitamin D levels to dysregulation of Th1/Th2 and Th17/Treg ratios. We summarized the effects of vitamin D on the immune system in BD.
      PubDate: 04/15/2014 12:15:02 pm
       
  • Nuclear-factor kB p65 is a mediator of insulin and tumour necrosis
           factor-alpha stimulated vascular cell adhesion molecule-1 expression in
           vascular endothelial cells.

    • Abstract: Introduction Type-2 Diabetes Mellitus (T2DM) is a combination of disorders that includes, but is not limited to, hyperinsulinemia, dyslipidemia and insulin resistance.  Among the sequelae of these pathologies are inflammation and atherosclerosis.   Whereas the canonical intracellular mediator of inflammation is Nuclear Factor kappa-B (NFkB), its role in atherosclerosis has not been fully characterized. Materials and methods Vascular cells were treated with either insulin (1 nM) or Tumor Necrosis Factor-alpha (TNFa) (1 ng/mL) alone or in combination in the absence or presence of intracellular kinase biochemical inhibitors or different isoforms of a genetic inhibitor of NFkB expression in order to determine changes in Vascular Cell Adhesion Molecule-1 expression.  Results We observed a considerable amount of cross-talk between kinases led to either significant decreases or increases in VCAM-1 expression, depending on the kinases inhibited.  Additionally, we determined that both insulin and TNFastimulated increases in VCAM-1 expression.  Yet, inhibition of two different intracellular kinase pathways had significantly different effects on insulin and TNFa-stimulated VCAM-1 expression.  Interestingly, only the p65 genetic inhibitor isoform of NFkB significantly decreased TNFa-stimulated VCAM-1 expression. In contrast, the p65 isoform genetic inhibitor moderately, but not significantly, effected insulin stimulated VCAM-1 expression. Conclusion Intracellular kinases are not single pathway mediators of extracellular signals to intracellular events, but are inter-related highways that communicate to each other to modulated cellular responses to their environment.  Interestingly, the expression of the cell surface adhesion molecule, VCAM-1, is in part mediated by the canonical mediator of inflammation, NFkB.  Although NFkB regulates TNFa-stimulated VCAM-1 expression, it does not mediate insulin-stimulated VCAM-1 expression.  This suggests that insulin-stimulated VCAM-1 expression is regulated in part by an NFkB-independent mediator, yet to be determined.
      PubDate: 04/15/2014 12:15:02 pm
       
  • The pathogenesis of cerebral vaso-spasm in bacterial meningitis.

    • Abstract: Introduction: Cerebral inflammation in bacterial meningitis has been associated with vasospasms of cerebral arteries and arterioles. Vasospasm has been associated with permanent neurological deficits and death. Objective of the review was to summarize the evidence for involvement of inflammatory mediators in the pathogenesis of cerebral vasospasm. Methods: Databases Pubmed, EMBASE and the Cochrane Library were searched and reference lists of retrieved articles using keywords including cerebral vasospasm, meningitis and inflammation. Results: Increased levels of interleukin-1 may be involved in vasospasm through release of the vasoconstrictor endothelin-1. Another key factor in the pathogenesis of cerebral arterial vasospasm may be the reduced bioavailability of the vasodilator nitric oxide. Therapeutic trials in vasospasm related to inflammation showed a reduction of vasospasm through calcium antagonists. The importance of inflammation in causing vasospasm has been highlighted by the successful reduction of features of vasospasm and morbidity by anti-inflammatory agents including steroids, and acetyl-salicylic acid which merit further study in all conditions with cerebral inflammation in double blind placebo controlled randomised trials. Conclusion: Key factors in the pathogenesis of cerebral vasospasm in bacterial meningitis are depletion of nitric oxide and effects of endothelin and interleukin-1. Auxiliary treatment increasing nitric oxide levels and antagonising the other inflammatory mediators may be able to reduce ischemic brain injury associated with neurological deficits and increased mortality in bacterial meningitis.
      PubDate: 04/15/2014 12:15:02 pm
       
  • A gap in cell death knowledge: Is necroptosis of eosinophils involved in
           allergic airway inflammation'

    • Abstract: Eosinophils are continually targeted in allergic airway inflammatory disease therapies while the presence of their granules in airway tissues remains unexplained, yet imply the involvement of necrosis. The latter’s definition has evolved into a highly regulated and distinct signaling pathway leading to physiological inflammation, known as necroptosis. Even though necroptosis is a recently introduced concept, we currently recognize its role as an alternative mechanism in the absence of apoptosis. Furthermore, necroptosis seems to act as a host defense strategy against viral infections, which consequently associates itself with eosinophils’ role in airway viral clearance. The investigation of necroptosis in eosinophil is currently an area of research which is lacking knowledge, yet harboring great promise for drug development.
      PubDate: 04/15/2014 12:15:02 pm
       
  • Seeing inflammation through the innate immune eye.

    • Abstract: Inflammation is triggered when innate immune cells detect microbial infection or tissue damage. Surveillance mechanisms involve pattern recognition receptors (PRRs) on the cell surface and in the cytoplasm. Most PRRs respond to pathogen-associated molecular patterns (PAMPs) or host-derived damage-associated molecular patterns (DAMPs) by triggering activation of various transcription factors. Induction of cytokines promotes the activation and recruitment of leukocytes, which are critical for eliminating pathogens and host debris. In order to avoid immunopathology, the system is very tightly regulated by numerous molecules that limit the magnitude and duration of the inflammatory response. In this review we present current knowledge on pathogen recognition through different PRRs and the complex signaling pathways responsible for activation of inflammatory and antimicrobial responses.
      PubDate: 04/15/2014 12:15:02 pm
       
  • Defining the therapeutic and preventative anti-inflammatory benefits of
           curcumin in vitro.

    • Abstract: Introduction.In the setting of inflammatory bowel disease, curcumin supplementation to prevent inflammatory flares has shown promise. However the outcome of curcumin exposure when there is existing inflammation is not clear. The aim of this study was to compare the anti-inflammatory properties of curcumin when added at differing times to an inflammatory stimulus, in an established in vitro intestinal epithelial cell model of intestinal inflammation. Methods. HT29 and INT407 cells were incubated with a range of concentrations of curcumin prior to, or at the same time as, the addition of TNF-α. Following incubation, cell viability, interleukin-8 levels and cytoplasmic IκB were assessed. Results. High concentrations of curcumin reduced epithelial cell viability. At lower concentrations curcumin had no effect on cell viability, however curcumin (with or without pre-incubation) reduced IL-8 levels and inhibited the phosphorylation and of degradation of IκB. Conclusion.Curcumin can reduce the IL-8 and IκBresponse to TNF-α in an invitromodel of intestinal inflammation. This response is not dependent on curcumin pre-incubation but does depend on curcumin concentration. These finding supports the role of curcumin as an anti-inflammatory therapy and suggest it may be effective in both reducing existing inflammation and preventing inflammatory relapse. Further research is needed to assess optimal in vivo curcumin dosing.
      PubDate: 04/15/2014 12:15:02 pm
       
  • The transient receptor potential melastatin-2 (TRPM2) channel and
           inflammation.

    • Abstract: Inflammation is an early mechanism of the immune system to eliminate pathogens and to repair damaged tissue. However, unregulated and persistent inflammation can lead to chronic inflammatory diseases. The transient receptor potential melastatin-2 (TRPM2) channel, a calcium (Ca2+)-permeable channel containing intracellular adenosine diphosphate ribose (ADPR) pyrohydrolase activity, has recently been identified as a critical molecular mechanism in reactive oxygen species (ROS)-induced inflammatory process, and thereby, emerged as a potential target for therapeutic intervention. ADPR biding to TRPM2 Nudix-like domain (or NUDT9 homology domain) results in the channel pore opening allowing lysosomal Ca2+ release and Ca2+ influx into the cells. Ca2+ influx via TRPM2 controls ROS-induced nuclear translocation of NF-kB and CXCL2 production in monocytes during inflammation in a chronic experimental colitis mouse model. Moreover, TRPM2 deficient-dendritic cells show defective Ca2+ signals and chemotaxis toward CXC12 and CCL21 chemokines. TRPM2-/- mice are also more susceptible to Listeria monocytogenes infection. In contrast, TRPM2 is not required for airway inflammation in OVA-induced allergic asthma and in chronic obstructive pulmonary disease in mice. Consequently, TRPM2 appears to play a role in chronic inflammation and might not participate in acute inflammatory responses.
      PubDate: 04/15/2014 12:15:02 pm
       
 
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