DOI: 10.29245/2578-3009/2018/3.1136 View / Download Pdf View Full Text
1Lipidology and Center for Extracorporeal Treatment, Department of Internal Medicine III, University Hospital Carl Gustav Carus at the Technische Universität Dresden, Germany Fetscherstr. 74, 01307 Dresden (Germany)
DOI: 10.29245/2578-3009/2018/3.1133 View / Download Pdf View Full Text
Wee Kiat Tan1, Johan CK Tay2, Jieming Zeng3, Min Zheng4, Shu Wang2,3*
1Tessa Therapeutics, Pte Ltd., Singapore 239351
2Department of Biological Sciences, National University of Singapore, Singapore 117543
3Institute of Bioengineering and Nanotechnology, Singapore 138669
4Department of Dermatology, Second Affiliated Hospital, Zhejiang University, School of Medicine, China 310009
Emmanuel E. Ekanem1*, Joanan M. Ikobah1, Henry C. Okpara2
1DEPARTMENT OF PAEDIATRICS, UNIVERSITY OF CALABAR AND UNIVERSITY OF CALABAR TEACHING HOSPITAL, CALABAR, NIGERIA.
2DEPARTMENT OF CHEMICAL PATHOLOGY, UNIVERSITY OF CALABAR AND UNIVERSITY OF CALABAR TEACHING HOSPITAL, NIGERIA.
The faeco-orally transmitted hepatotropic viruses – hepatitis A and hepatitis E viruses- are endemic in Africa. While transmission has reduced remarkbly in Europe and North America in the past decades, it has remained unchanged in Africa with hepatitis A prevalence remaining at above 50% and hepatitis E more than 7%. Much of this transmission occurs during childhood with the important drivers/predictors being poor water supply, poor sewage disposal facilities, low socioeconomic class, crowding, and poor social conditions arising from conflict. Initial clinical features in children are difficult to distinguish from malaria which is also endemic in the region. Commercially available ELISA kits present the best option for laboratory diagnosis of both viruses in Africa. While effective vaccines suitable for the African situation have been developed recently, improved water supply and sanitation are sine qua non for the prevention of transmission of both viruses among African children. Interventional studies are needed in the region.DOI: 10.29245/2578-3009/2018/3.1138 View / Download Pdf View Full Text
DOI: 10.29245/2578-3009/2018/3.1141 View / Download Pdf View Full Text
María Virginia Croce1*, Martín E. Rabassa1, Amada Segal-Eiras1
1Centre of Basic and Applied Immunological Research (CINIBA), Faculty of Medical Sciences, National University of La Plata, Argentina.
Mahmoud M. Bakr1, Simon Guan2, Norman Firth3, Robert M. Love1*
1School of Dentistry and Oral Health, Griffith University, Australia
2School of Dentistry, University of Otago, New Zealand
3University of Queensland, Brisbane, Australia
There is increasing evidence suggesting that cyclins, cyclin-dependent kinases (CDKs), and cyclin-dependent kinase inhibitors (CDIs) either are themselves targets for genetic change in cancer or are disrupted secondarily by other oncogenic events. Cyclin D1 and p27KIP1 are two important regulators at the G1/S checkpoint. Cyclin D1 is an oncogene of cell cycle regulation with positive effect. Normally, cyclin D1 at G1 is constant or at a very low level and its excessive expression may be associated with the disordered proliferation of cells leading to malignant change. On the other hand, p27KIP1 is an anti-oncogene for cell cycle regulation, which functions as a negative regulator. Under the regulation of TGF-β, p27KIP1 inhibits the activity of oncogenes and controls the transition of the G1/S phase mainly by the interaction with CDK and CDK-Cyclin in order to inhibit cell proliferation and give cells opportunities to repair DNA. In addition, p27KIP1 not only acts as CDK inhibitor, but also promotes cell differentiation and induces the apoptosis of cells. In this article we review studies that have explored the effects of cyclin D1 and P27KIP1 on cancer progression and dysplasia with a specific focus on oral dysplasia and oral squamous cell carcinoma (OSCC). We also aim to shed some light on the different means of evaluating the interaction between Cyclin D1 and P27KIP1 as well as the immunohistochemical reactions associated with different forms of cyclin D1.DOI: 10.29245/2578-3009/2018/3.1142 View / Download Pdf View Full Text
Kazuhiko Hashimoto1*, Yutaka Oda1, Kotaro Yamagishi1, Ichiro Tsukamoto1, Masao Akagi1
1Department of Orthopedic Surgery, Kindai University Hospital, Osaka-Sayama City, Osaka 589-8511, Japan
Background: Some reports have shown that metabolic syndrome, including hypertension, hyperlipidemia, and diabetes mellitus, contributes to osteoarthritis (OA) development. Further, lectin-like oxidized low-density lipoprotein (ox-LDL) and ox-LDL receptor-1 (LOX-1), which contributes to atherosclerosis, have also been considered factors contributing to OA development. Several studies have suggested that the LOX-1/ox-LDL system is involved in OA development in vitro. We have suggested the same and conducted in vitro and in vivo studies to validate this concept. However, the role of the LOX-1/ox-LDL system in OA development has not been clarified. This study aimed to identify the mechanism of the LOX-1/ox-LDL system to clarify OA development.
Methods: A zymosan-induced arthritis model was used to identify the mechanism of the LOX-1/ox-LDL system using LOX-1-knockout (KO) mice. Zymosan was administered via the intra-articular route to induce arthritis.
Results: From our experiment, we found that the LOX-1/ox-LDL system contributes to OA development through matrix metalloproteinase-3.
Conclusion: Our findings suggest that the treatment of abnormal lipid metabolism may contribute to the prevention and suppression of arthritis.DOI: 10.29245/2578-3009/2018/3.1139 View / Download Pdf View Full Text
1Emergency Department, Humanitas Research Hospital, Via Manzoni 56, 20089 Rozzano, Italy
The term post-cardiac injury syndrome (PCIS) defines a group of inflammatory diseases involving predominantly the pericardium. The syndrome results from a cardiac injury and refers mainly to post-myocardial infarction pericarditis, post-pericardiotomy syndrome and post-traumatic pericarditis (including iatrogenic conditions appearing after percutaneous interventions).
Signs and symptoms are similar to those seen in acute pericarditis and pericardial effusion in other clinical settings. The diagnosis is clinical and could be challenging in the Emergency Department (ED). PCIS should be considered as an alternative diagnosis to acute pericarditis in case of unilateral right-sided, massive, or transudative pleural effusion.
Although typically a benign condition, PCIS may result in significant morbidity and potential mortality; tamponade and constrictive pericarditis represent the leading complications. Therefore, early detection is clinically relevant. Currently, a combination of nonsteroidal anti-inflammatory drugs and colchicine is the mainstay treatment for this condition. Colchicine has also appeared to be effective in primary prevention of PCIS after cardiac surgery.
The purpose of this article is to review the principle clinical characteristics of PCIS in order to achieve an early diagnosis.DOI: 10.29245/2578-3009/2018/3.1127 View / Download Pdf View Full Text
Ana Cirac1,2,3, Uta Behrends1,2,3, and Josef Mautner1,2,3*
1Children’s Hospital, Technische Universität München, Munich, Germany
2Research Unit Gene Vectors, Helmholtz Zentrum München, Munich, Germany
2German Centre for Infection Research (DZIF), partner site Munich, Germany
The Epstein-Barr virus (EBV), a ubiquitous γ-herpesvirus, has been implicated in the etiology of several acute and chronic inflammatory, autoimmune, and malignant diseases. Although considered a genetically stable virus, recent sequence information obtained from a large number of viral isolates from around the world revealed that numerous viral variants exist. Whether these different strains differ in pathogenicity and immunogenicity and thereby contribute to the varying incidence rates of several EBV-associated diseases in different geographical regions is now studied intensively. The recent identification of amino acid sequence polymorphisms in a high percentage of all known virus-specific CD4+ and CD8+ T-cell epitopes, and of holes in the individual T-cell repertoire against epitopes derived from strain variants, may suggest that antiviral immunity is incompletely cross-protective against diverse EBV strains. These findings may have implications for immunological approaches seeking to prevent, monitor, or treat EBV-associated diseases.DOI: 10.29245/2578-3009/2018/3.1145 View / Download Pdf View Full Text
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Wilma Carvalho Neves Forte1*, Tainá Mosca1
1Immunology Discipline, Santa Casa de Sao Paulo School of Medical Sciences, São Paulo, SP, Brazil
Jheng-Yu Wu1, 2, Niko Moses1,2, Wenlong Bai3, Xiaohong Mary Zhang1,2*
1Department of Oncology, Molecular Therapeutics Program, Karmanos Cancer Institute, Detroit, Michigan 48201
2Wayne State University School of Medicine, Detroit, Michigan 48201
3Department of Pathology and Cell Biology, Morsani College of Medicine, University of South Florida, Tampa, FL 33612
The oncogene HDAC6 controls numerous cell processes that are related to tumorigenesis and metastasis, and has recently arisen as a target to treat malignancies. The ERK cascade is a classic pathway driving oncogenesis, and the components of this pathway are either highly mutated in cancers or are vital in cancer’s pathological activity. The interactions between these important components of tumor proliferation have been examined, and our research has demonstrated that they regulate each other as evidenced by different posttranslational modifications. Preclinical evidence also supports clinical trials cotargeting these two pathways, which may provide better efficacy than single treatment. Furthermore, HDAC6 and ERK both participate in the regulation of T cell maturation and may have implications on the functions of immune cells. This leads to the possibility of connecting HDAC6 and ERK to immunotherapy. In this review, we summarize the published studies about the interaction of HDAC6 and ERK cascade and their relationship to cancers. We also include the association of HDAC6 and ERK to immune system and discuss the plausibility of linking these to immunotherapy.DOI: 10.29245/2578-3009/2018/3.1143 View / Download Pdf View Full Text
Godfrey S. Getz1* and Catherine A. Reardon2
1Department of Pathology, The University of Chicago, Chicago, IL 60637, USA
2Ben May Institute for Cancer Research, The University of Chicago, Chicago, IL 60637, USA
Atherosclerosis is the underlying basis for most cardiovascular diseases. It is a chronic inflammation affecting the arterial intima and is promoted by hypercholesterolemia. Cells of both the innate and adaptive immune systems contribute to this inflammation with macrophages and T cells being the most abundant immune cells in the atherosclerotic plaques. In this review, we discuss the studies that examined the role of T cells and T cell subsets in Apoe-/- and Ldlr-/- murine models of atherosclerosis. While there is a general consensus that Th1 cells are pro-atherogenic and regulatory T cells are atheroprotective, the role of other subsets is more ambiguous. In addition, the results in the two models of atherosclerosis do not always yield similar results. Additional studies in the two murine models using cell specific gene manipulations are needed.DOI: 10.29245/2578-3009/2018/3.1144 View / Download Pdf View Full Text