Relevant bibliographies by topics / Metalloproteinases Inhibitors Therapeutic use

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Academic literature on the topic 'Metalloproteinases Inhibitors Therapeutic use'

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Published: 4 June 2021
Last updated: 28 January 2023

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Journal articles on the topic "Metalloproteinases Inhibitors Therapeutic use"

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Ganea, E., M. Trifan, A. C. Laslo, G. Putina, and C. Cristescu. "Matrix metalloproteinases: useful and deleterious." Biochemical Society Transactions 35, no. 4 (July 20, 2007): 689–91. http://dx.doi.org/10.1042/bst0350689.

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MMPs (matrix metalloproteinases) are zinc-dependent endopeptidases that degrade both matrix and non-matrix proteins. They play an important role in morphogenesis, and in a wide range of processes including tissue repair and remodelling. Their abnormal expression contributes to pathological processes including arthritis, cancer, and cardiac and central nervous system diseases, which explains the large interest in finding specific MMP inhibitors for therapeutic use. In this review we describe the structural features of MMPs, with special emphasis on their interaction with specific inhibitors. The effect of new, hydroxamatebased inhibitors on MMP isolated from bovine brain is evaluated.
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Jakubowska, Katarzyna, Anna Pryczynicz, Piotr Iwanowicz, Andrzej Niewiński, Elżbieta Maciorkowska, Jerzy Hapanowicz, Dorota Jagodzińska, Andrzej Kemona, and Katarzyna Guzińska-Ustymowicz. "Expressions of Matrix Metalloproteinases (MMP-2, MMP-7, and MMP-9) and Their Inhibitors (TIMP-1, TIMP-2) in Inflammatory Bowel Diseases." Gastroenterology Research and Practice 2016 (2016): 1–7. http://dx.doi.org/10.1155/2016/2456179.

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Crohn’s disease (CD) and ulcerative colitis (UC) belong to a group of inflammatory bowel diseases (IBD). The aim of our study was to evaluate the expression of MMP-2, MMP-7, MMP-9, TIMP-1, and TIMP-2 in ulcerative colitis and Crohn’s disease. The study group comprised 34 patients with UC and 10 patients with CD. Evaluation of MMP-2, MMP-7, MMP-9, TIMP-1, and TIMP-2 expression in tissue samples was performed using immunohistochemistry. The overexpression of MMP-9 and TIMP-1 was dominant in both the glandular epithelium and inflammatory infiltration in UC patients. In contrast, in CD subjects the positive expression of MMP-2 and TIMP-1 was in glandular tubes while mainly MMP-7 and TIMP-2 expression was in inflammatory infiltration. Metalloproteinases’ expression was associated with the presence of erosions, architectural tissue changes, and inflammatory infiltration in the lamina propria of UC patients. The expression of metalloproteinase inhibitors correlated with the presence of eosinophils and neutrophils in UC and granulomas in CD patients. Our studies indicate that the overexpression of metalloproteinases and weaker expression of their inhibitors may determine the development of IBD. It appears that MMP-2, MMP-7, and MMP-9 may be a potential therapeutic target and the use of their inhibitors may significantly reduce UC progression.
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De, S., J. E. Fenton, and A. S. Jones. "Matrix metalloproteinases and their inhibitors in non-neoplastic otorhinolaryngological disease." Journal of Laryngology & Otology 119, no. 6 (June 2005): 436–42. http://dx.doi.org/10.1258/0022215054273269.

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Matrix metalloproteinases (MMPs) are a family of zinc and calcium-dependent endopeptidases that play a key role in extracellular matrix (ECM) degradation. MMPs are known to be important in normal remodelling processes. Overexpression and activation of MMPs or an imbalance of active MMPs and tissue inhibitors of metalloproteinases (TIMPs) has been linked with a number of specific disease states associated with the breakdown and remodelling of the extracellular matrix. MMPs and TIMPs play a role in the development and progression of conditions such as acute and chronic otitis media, nasal polyposis and Sjogren’s disease of salivary glands. Their role in allergic rhinitis has not been proven although they do appear to have a role in asthma, a condition closely linked to rhinitis. The use of a broad spectrum MMP inhibitor has been shown to alter the outcome of acute otitis media and otitis media with effusion. Therapeutic strategies with anti-MMP molecules are currently being developed and may play a role in modulating the course of non-neoplastic otorhinolaryngological disease in the future.
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Titovska, S. O. "EFFECTIVENESS OF MATRIX METALLOPROTEINASES INHIBITORS FOR PREVENTIVE TREATMENT OF GENERALIZED PERIODONTITIS." Ukrainian Dental Almanac, no. 2 (June 27, 2022): 10–15. http://dx.doi.org/10.31718/2409-0255.2.2022.02.

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Generalized periodontitis is one of the most widespread human stomatological diseases; it is diagnosed in 11.0 % of the world's population. Despite the recognition of the microbial factor as leading in its etiopathogenesis, antimicrobial treatment of gingivitis, added with removal of dental plaque, does not prevent the further development of periodontitis. Dysbacteriosis causes inflammation which leads to an increase of proteolysis products. They are a nutrient medium for periodontal pathogenic microflora, they contribute to its growth. So, the use of anti-inflammatory drugs, such as matrix metalloproteinase inhibitors, is promising for preventive treatment of generalized periodontitis. The aim of the work is to conduct a clinical trial of complex treatment which includes matrix metalloproteinase inhibitors in patients with diffuse gingivitis and generalized periodontitis of chronic course. Materials and methods of the research. 60 patients with chronic course of diffuse gingivitis and generalized periodontitis of initial, I and II stages, were treated. The effectiveness of the treatment was evaluated in the early and distant term (after 1 year) according to data of the clinical and radiological examination, computer tomography, biochemical examination of oral fluid for matrix metalloproteinases-8 and -9 (MMP-8, -9) and immunohistochemical study of gingival biopsies for cytoplasmic expression of matrix metalloproteinase-1 (MMP-1). Results of the research. According to the data of the clinical examination, complete elimination of inflammatory symptoms in periodontal tissues was achieved in 93.3% of patients in the comparison group in 12-14 days and in 96.7% in the base group in 10-12 days. In patients in whom the developed therapeutic scheme was used, the best dynamics of the index assessment of the state of hygiene, gingiva and periodontal complex was established. The main difference between the research groups was the preservation of obtained results in 1 year after treatment in patients of the base group (p ˂ 0.05). In particular, a year later, the results of bone mineral density measurement for patients of the base group did not change from baseline, while in the comparison group there was their significant decrease (p ˂ 0.05), indicating the progression of inflammatory-destructive process in periodontal tissues. After treatment, a significant reduction in the level of MMP-8 and MMP-9 in the oral fluid of patients of both groups was achieved (p ˂ 0.05). In patients of the base group, in contrast to the comparison, these results were the same in the distant term (p ˂ 0.05). When assessing the cytoplasmic expression of MMP-1 in epithelial and stromal cells after treatment, zero result was in 96.7% of patients in the base group and in 80.0% – in the comparison group, and after 1 year – in 90.0% vs 63.3% respectively. It should be noted that the differences between the base and comparison groups were most observed for patients with gingivitis and generalized periodontitis of initial stage without destructive processes in periodontal tissues. It suggests the greatest effectiveness of the proposed treatment in the early stages of pathological process. Thus, based on the fact that the activity of matrix metalloproteinases characterizes the course of the inflammatory process in periodontal tissues, a decrease in their level according to biochemical and immunohistochemical studies in the base group against the comparison indicates a better anti-inflammatory effect of the developed treatment to prevent the progression of generalized periodontitis. Conclusion. The obtained results allow recommending the use of matrix metalloproteinase inhibitors as a preventive pathogenetic treatment for the patients with chronical course of gingivitis and generalized periodontitis of the initial stage, to inhibit the inflammatory component of the pathological process. Prospects for further research. It should be studied the indication for repeated courses of matrix metalloproteinase inhibitors in patients with periodontal disease.
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Beletskaya, Inessa Stanislavovna, and Sergey Yurievich Astakhov. "The role of matrix metalloproteinases in glaucoma pathogenesis." Ophthalmology journal 8, no. 3 (December 15, 2015): 28–43. http://dx.doi.org/10.17816/ov2015328-43.

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Matrix metalloproteinases belong to an enzyme family, which assure a proteolysis of practically all components of the extracellular matrix of connective tissues in normal and pathological conditions. At physiological conditions, there are evidences on the impact of this enzyme group in the embryogenesis, morphogenesis, angiogenesis, and tissue involution. The activity impairment of matrix metalloproteinases and of their specific inhibitors leads to the biosynthesis misbalance and to the degradation of extracellular matrix components; it plays a role in the development of such diseases as diabetes mellitus, rheumatoid arthritis, and arteriosclerosis. Laboratory tests and clinical investigation results confirm the role of these enzymes in tissue remodeling of different eyeball structures in glaucoma (in particular, of the trabecular meshwork and the optic disc); it leads to intraocular fluid outflow impairment and to the glaucomatous optic neuropathy development. In the review, the analysis of clinical and experimental studies is performed that are dedicated to the investigation of matrix metalloproteinases role in the pathogenesis of different glaucoma types, of the possibility to use them as biomarkers, as well as therapeutic action targets in this disease.
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Docherty, Andy J., Tom Crabbe, James P. O'Connell, and Colin R. Groom. "Proteases as drug targets." Biochemical Society Symposia 70 (September 1, 2003): 147–61. http://dx.doi.org/10.1042/bss0700147.

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The effective management of AIDS with HIV protease inhibitors, or the use of angiotensin-converting enzyme inhibitors to treat hypertension, indicates that proteases do make good drug targets. On the other hand, matrix metalloproteinase (MMP) inhibitors from several companies have failed in both cancer and rheumatoid arthritis clinical trials. Mindful of the MMP inhibitor experience, this chapter explores how tractable proteases are as drug targets from a chemistry perspective. It examines the recent success of other classes of drug for the treatment of rheumatoid arthritis, and highlights the need to consider where putative targets lie on pathophysiological pathways--regardless of what kind of therapeutic entity would be required to target them. With genome research yielding many possible new drug targets, it explores the likelihood of discovering proteolytic enzymes that are causally responsible for disease processes and that might therefore make better targets, especially if they lead to the development of drugs that can be administered orally. It also considers the impact that biologics are having on drug discovery, and in particular whether biologically derived therapeutics such as antibodies are likely to significantly alter the way we view proteases as targets and the methods used to discover therapeutic inhibitors.
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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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Doll, Carla U., Sabine Niebert, and Janina Burk. "Mesenchymal Stromal Cells Adapt to Chronic Tendon Disease Environment with an Initial Reduction in Matrix Remodeling." International Journal of Molecular Sciences 22, no. 23 (November 26, 2021): 12798. http://dx.doi.org/10.3390/ijms222312798.

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Tendon lesions are common sporting injuries in humans and horses alike. The healing process of acute tendon lesions frequently results in fibrosis and chronic disease. In horses, local mesenchymal stromal cell (MSC) injection is an accepted therapeutic strategy with positive influence on acute lesions. Concerning the use of MSCs in chronic tendon disease, data are scarce but suggest less therapeutic benefit. However, it has been shown that MSCs can have a positive effect on fibrotic tissue. Therefore, we aimed to elucidate the interplay of MSCs and healthy or chronically diseased tendon matrix. Equine MSCs were cultured either as cell aggregates or on scaffolds from healthy or diseased equine tendons. Higher expression of tendon-related matrix genes and tissue inhibitors of metalloproteinases (TIMPs) was found in aggregate cultures. However, the tenogenic transcription factor scleraxis was upregulated on healthy and diseased tendon scaffolds. Matrix metalloproteinase (MMPs) expression and activity were highest in healthy scaffold cultures but showed a strong transient decrease in diseased scaffold cultures. The release of glycosaminoglycan and collagen was also higher in scaffold cultures, even more so in those with tendon disease. This study points to an early suppression of MSC matrix remodeling activity by diseased tendon matrix, while tenogenic differentiation remained unaffected.
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Cho, Chul-Hyun, Kwang-Soon Song, Beom-Soo Kim, Du Hwan Kim, and Yun-Mee Lho. "Biological Aspect of Pathophysiology for Frozen Shoulder." BioMed Research International 2018 (2018): 1–8. http://dx.doi.org/10.1155/2018/7274517.

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It is fairly well understood that frozen shoulder involves several stages, which reflect the series of process from capsular inflammation and fibrosis to spontaneous resolution of this fibrosis. However, the underlying pathophysiologic process remains poorly determined. For this reason, management of frozen shoulder remains controversial. Determining the pathophysiological processes of frozen shoulder is a pivotal milestone in the development of novel treatment for patients with frozen shoulder. This article reviews what is known to date about the biological pathophysiology of frozen shoulder. Although articles for the pathophysiology of frozen shoulder provide inconsistent and inconclusive results, they have suggested both inflammation and fibrosis mediated by cytokines, growth factors, matrix metalloproteinases, and immune cells. Proinflammatory cytokines and growth factors released from immune cells control the action of fibroblast and matrix remodeling is regulated by the matrix metalloproteinases and their inhibitors. To improve our understanding of the disease continuum, better characterizing the biology of these processes at clearly defined stages will be needed. Further basic studies that use standardized protocols are required to more narrowly identify the role of cytokines, growth factors, matrix metalloproteinases, and immune cells. The results of these studies will provide needed clarity into the control mechanism of the pathogenesis of frozen shoulder and help identify new therapeutic targets for its treatment.
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Laghezza, Antonio, Luca Piemontese, Leonardo Brunetti, Alessia Caradonna, Mariangela Agamennone, Fulvio Loiodice, and Paolo Tortorella. "(2-Aminobenzothiazole)-Methyl-1,1-Bisphosphonic Acids: Targeting Matrix Metalloproteinase 13 Inhibition to the Bone." Pharmaceuticals 14, no. 2 (January 24, 2021): 85. http://dx.doi.org/10.3390/ph14020085.

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Matrix Metalloproteinases (MMPs) are a family of secreted and membrane-bound enzymes, of which 24 isoforms are known in humans. These enzymes degrade the proteins of the extracellular matrix and play a role of utmost importance in the physiological remodeling of all tissues. However, certain MMPs, such as MMP-2, -9, and -13, can be overexpressed in pathological states, including cancer and metastasis. Consequently, the development of MMP inhibitors (MMPIs) has been explored for a long time as a strategy to prevent and hinder metastatic growth, but the important side effects linked to promiscuous inhibition of MMPs prevented the clinical use of MMPIs. Therefore, several strategies were proposed to improve the therapeutic profile of this pharmaceutical class, including improved selectivity toward specific MMP isoforms and targeting of specific organs and tissues. Combining both approaches, we conducted the synthesis and preliminary biological evaluation of a series of (2-aminobenzothiazole)-methyl-1,1-bisphosphonic acids active as selective inhibitors of MMP-13 via in vitro and in silico studies, which could prove useful for the treatment of bone metastases thanks to the bone-targeting capabilities granted by the bisphosphonic acid group.
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Dissertations / Theses on the topic "Metalloproteinases Inhibitors Therapeutic use"

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Tang, Wing-yan, and 鄧詠欣. "Curcumin inhibits cancer cells migration and invasion of tongue carcinoma through down-regulation of matrix metalloproteinase-10." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2012. http://hub.hku.hk/bib/B47869768.

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 Squamous cell carcinoma of the tongue has a low survival rate, with cure rate reduced by half if cervical lymph node metastasis is present. Standard treatment regimen includes surgical resection of the tumor, radiotherapy and chemotherapy. These treatment modalities, however, can result in irreversible side effects including loss of form and function of the tongue. So far, there is no efficient treatment regime targeting migration and invasion of tongue carcinoma. Curcumin is a natural polyphenol extracted from Curcuma longa. Recent studies indicated that curcumin is a potential anti-cancer agent. The anticancer effects have been demonstrated in numerous cancers including lung cancer, liver cancer, breast cancer, prostate cancer and melanoma. In head and neck cancers, the number studies is limited and its inhibitory effects in migration and invasion is rarely explored. To explore the global expression changes in tongue cancer, we used microarray to evaluate the genes responsive to curcumin treatment and focused on genes related to migration and invasion of tongue cancer cell line HN21B. The genes down-regulated by curcumin were validated in HN21B and two other tongue cancer cell line CAL27 and HN96 using qRT-PCR, Western blotting and immunostaining. The identified genes were quantified in tongue carcinoma tissues to examine whether it was up-regulated in human tongue tissues. Scratch wound assay and radial-migration assay were used to assess the degree of inhibition on migration. Adhesion and invasion assays were also performed to assess the adhesion and invasion ability. Transcriptomic analyses showed that MMP-10 was 2.36 fold down-regulated in HN21B in response to curcumin. Curcumin treatment resulted in down-regulation of MMP-10 gene in all the 3 tongue carcinoma cell lines at mRNA and protein levels. Out of 24 tongue carcinoma cases, 55% tumor tissue had obvious up-regulation of MMP-10 expression in comparison with the normal counterpart. Adhesion, migration and invasion ability of tongue carcinoma cell lines was significantly reduced upon IC50 of curcumin treatment in all TSCC cell lines. In conclusion, our results indicated that curcumin could reduce migration, adhesion and invasion in tongue carcinoma cells partly through reducing MMP-10 expression. Further investigations are warranted to explore the potential therapeutic use of curcumin to inhibit migration and invasion of tongue carcinoma cells.
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Surgery
Master
Master of Philosophy
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2

Roach, Denise Margaret. "Upregulation of matrix metalloproteinases -2 and -9 and type IV collagen degradation in skeletal muscle reperfusion injury." Title page, contents and abstract only, 2002. http://web4.library.adelaide.edu.au/theses/09MD/09mdr6281.pdf.

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Includes bibliographical references (leaves 292-352) Determines the role of matrix metalloproteinases, MMP-2 and MMP-9 in reperfusion injury following skeletal muscle ischaemia; and, whether inhibition of MMPs by doxycycline protects against tissue damage.
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3

Peng, Xiaofang, and 彭晓芳. "Naturally occurring inhibitors against the formation of advanced glycation endproducts." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2010. http://hub.hku.hk/bib/B44892706.

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Sun, Wentao, and 孙文韬. "The effects of Panax notoginseng extracts and its components on TNF-alpha induced MMP-9 expression and activity." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2014. http://hdl.handle.net/10722/207686.

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Matrix metalloproteinase (MMP) induced extra cellular matrix (ECM) degradation is a crucial process involved in the development of many chronic inflammatory diseases, including cardiac remodeling and cancer metastasis. In cardiac remodeling, the presence of pathological stimuli leads to elevated MMP-9 expression and impairment of cardiac performance, which subsequently develops into heart failure. While in tumorgenesis, MMP-9 has been found to play key roles in metastasis, as it can break physical barriers for the tumor. Therefore, searching for agents targeting MMP-9 is a new direction for the treatment of cardiac remodeling and cancer metastasis. Chinese herbal medicine is becoming increasingly used worldwide in recent decades. In the past twenty years, as many highly selective and sensitive bioassays were introduced into the bioactive compounds screening from herbal medicine, more than one hundred new drug candidates have been identified. Therefore, herbal medicine is a potential source of bioactive compounds. Panax notoginseng (PNG) is one of the most common traditional Chinese medicines to treat cardiovascular diseases, and it was also reported to have anti-cancer effect. We hypothesized that it contains bioactive compounds that could inhibit MMP-9 activity in cardiomyocytes and cancer cells. In order to examine the effect of PNG on cardiac remodeling and cancer metastasis, we employed TNF-α induced MMP-9 in H9c2 cell (a rat cardiomyocyte) and HepG-2 cell (a human hepatoma cell) as an in vitro assay, respectively. PNG was first extracted by four different extraction methods according to the polarity of the solvent. The most effective fraction in suppressing MMP-9 activity in TNF-α induced H9c2 cell was chosen for further separation by silica gel column chromatography and high performance liquid chromatography (HPLC) until a single compound was isolated. According to the result of spectroscopic analysis by NMR, the compound was identified as ginsenoside Rb1. For the bioactivity assays, real-time quantitative polymerase chain reaction (QPCR) and Enzyme-linked immunosorbent assay (ELISA) were used to measure the mRNA and protein expression of MMP-9, respectively. We also examined the MMP-9 activity by gelatin zymography. The results showed that both of the PNG extract obtained from 10% ethanol extraction method (PNG-3) and purified Compound P (ginsenoside Rb1) showed significant inhibitory effect on MMP-9 expression and activity in H9c2 cells and HepG-2 cells. We further examined the molecular mechanisms of the inhibitory effect of PNG-3. H9c2 and HepG-2 cells were pretreated with different kinase inhibitors followed by the activation by TNF-α. The results showed the protein kinase R (PKR) inhibitor could inhibit TNF-α induced MMP-9 in both of the two cell lines. Furthermore, the results of Western blot showed the PNG-3 suppressed the phosphorylation of eIF-2α which is a down-stream effector of PKR in TNF-α stimulated H9c2 and HepG-2 cells, respectively. Therefore, PNG-3 may act through PKR to regulate TNF-α induced MMP-9 activity. In summary, bioactivity guided fractionation is an effective way of isolating bioactive compounds from medicinal herbs. In addition, PNG containing ginsenoside Rb1 may be a potential candidate of MMP-9 inhibition for the treatment of cardiac remodeling and cancer metastasis.
published_or_final_version
Paediatrics and Adolescent Medicine
Master
Master of Philosophy
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5

Chan, Hoi-ching, and 陳凱靜. "Heat shock protein 90 inhibitor 17-AAG potentiates anticancer activityof bortezomib in NK cell malignancies." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2011. http://hub.hku.hk/bib/B46632025.

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He, Ru, and 何茹. "Effectiveness and toxicity of aromatase inhabitors [i.e. inhibitors] in adjuvant therapy for hormone receptor positive postmenopausalbreast cancer: a meta-analysis." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2011. http://hub.hku.hk/bib/B46936026.

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Gu, Baoying. "Selective increase of neuronal cyclooxygenase-2 (COX-2) expression in vulnerable brain regions of rats with experimental Wernicke's encephalopathy : effects of nimesulide." Thesis, McGill University, 2007. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=112627.

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Wernicke's encephalopathy is a neuropsychiatric disorder resulting from thiamine deficiency (TD) and is characterized by neuronal loss, astrocytic proliferation and microglial activation. Cyclooxygenases (COX) are enzymes which catalyze the first step in the synthesis of prostanoids. COX-1 is expressed constitutively and COX-2 is the inducible isoform. Groups of TD rats and pair-fed controls were killed at presymptomatic and symptomatic stages of encephalopathy. Cresyl violet and NeuN staining showed decreased numbers of neuronal cells in vulnerable regions (medial thalamus and inferior colliculus) but not in a spared region (frontal cortex). Numbers of GFAP-positive and OX-42-positive cells were increased at symptomatic stage of encephalopathy. Expression of COX-2 mRNA and neuronal COX-2 immunoreactivity were selectively increased in vulnerable regions of TD rats at symptomatic stages of encephalopathy. Nimesulide, a highly selective COX-2 inhibitor, lowered PGE2 levels and precipitated the progression of encephalopathy suggesting that COX-2 in this model is conferring neuroprotection.
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Ho, Kwun-wai, and 何冠威. "Angiotensin converting enzyme inhibitor alone or in combination with angiotensin II type I receptor blocker in patients with chronicproteinuric nephropathies: a systemic reviewof clinical trials." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2005. http://hub.hku.hk/bib/B45010687.

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Scrivens, Paul James. "Regulation and chemotherapeutic targeting of human Cdc25A phosphatase." Thesis, McGill University, 2007. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=103293.

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The Cdc25 phosphatases are highly conserved from yeast through humans and play pivotal roles in regulating the activities of cyclin-dependent kinases (Cdks). Cdc25A is one of three human Cdc25 family members, and has previously been shown to be overexpressed in numerous cancers and to transform rodent fibroblasts. Cdc25A therefore represents a rational target for chemotherapeutic development. Further, a thorough understanding of its biology and regulation in normal and transformed cells may facilitate the development of strategies to specifically interfere with the proliferation of cancerous cells. In this work I describe experiments which demonstrate that bisperoxoVanadium compounds, and specifically bpV(Me2Phen), inhibit Cdc25A phosphatase in vitro and in vivo. Further, these compounds cause cell-cycle arrest, are cytotoxic to cancer cells, and slow the growth of tumours in mouse models. With respect to the fundamental biology of Cdc25A, I have identified a sequence element (NLS) responsible for nuclear localization of Cdc25A phosphatase. An analysis of this sequence demonstrated high conservation of flanking phosphoacceptor sites, notably Serine 292. S292 was predicted to be a consensus PKA or CamKII substrate. Using site-directed mutagenesis I have shown that S292 is the sole site of PKA phosphorylation in vitro. The functional importance of S292 phosphorylation was investigated via transfections of phospho-mimetic mutants of S292 (S292E) expressed as GFP-fusion proteins; these studies indicate that S292 phosphorylation may promote nuclear localization. Studies by other groups have indicated that S292 is a phosphorylation site for inhibitory kinases, namely Chk1 and Chk2 (4). I generated a phospho-specific antibody to this site and demonstrate by immunofluorescence and western blotting an unexpected pattern of S292 phosphorylation associated with nuclear bodies and the mitotic apparatus. I provide evidence to suggest that these sites represent local fine-tuning of Cdc25A, allowing Cdk activity to be controlled at the level of specific subcellular structures. These studies highlight the complexity of Cdc25 regulation and indicate a previously unappreciated degree of control of their activity such that these enzymes exist in multiple discrete pools within a given cell.
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Wong, Carmen, and 黃嘉敏. "A systematic review of the drug sorafenib in extending survival time in patients with hepatocellular carcinoma." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2011. http://hub.hku.hk/bib/B46942865.

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Books on the topic "Metalloproteinases Inhibitors Therapeutic use"

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Rotheim, Philip. New developments in therapeutic enzyme inhibitors and receptor blockers. Norwalk, CT: Business Communications Co., 1996.

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Goudot-Perrot, Andrée. Metabolic inhibitors: Antibiotics - antimitotics - psychotropics. Stuttgart: Schwer Verlag, 1992.

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Co, Business Communications. New developments in therapeutic enzyme inhibitors and blockers. Norealk, CT: Business Communications Co., 2002.

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George, Weinbaum, Giles Ralph E, Krell Robert D, New York Academy of Sciences., and American Thoracic Society, eds. Pulmonary emphysema: The rationale for therapeutic intervention. New York, N.Y: New York Academy of Sciences, 1991.

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PhD, Henderson Brian, and Bodmer Mark W, eds. Therapeutic modulation of cytokines. Boca Raton, Fla: CRC Press, 1996.

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K, Ghosh Arun. Aspartic acid proteases as therapeutic targets. Weinheim: Wiley-VCH, 2010.

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K, Ghosh Arun. Aspartic acid proteases as therapeutic targets. Weinheim: Wiley-VCH, 2010.

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Philippe, Taupin, ed. The cystatin superfamily of proteinase inhibitors. New York: Nova Science Publishers, 2007.

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Osiadacz, Jarosław. Inhibitory topoizomeraz DNA i ich zastosowanie w chemioterapii. Wrocław: Oficyna Wydawnicza Politechniki Wrocławskiej, 1999.

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Li, William W. The antiangiogenic therapy self help book for cancer patients. Cambridge, Mass: Angiogenesis Foundation, 2003.

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Book chapters on the topic "Metalloproteinases Inhibitors Therapeutic use"

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Darby, Ian A., and Alexis Desmoulière. "Scar Formation: Cellular Mechanisms." In Textbook on Scar Management, 19–26. Cham: Springer International Publishing, 2020. http://dx.doi.org/10.1007/978-3-030-44766-3_3.

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AbstractFibroblasts are key players in the maintenance of skin homeostasis and in orchestrating physiological tissue repair. Fibroblasts secrete and are embedded in a sophisticated extracellular matrix, and a complex and interactive dialogue exists between fibroblasts and their microenvironment. In addition to the secretion of the extracellular matrix, fibroblasts and myofibroblasts secrete extracellular matrix remodeling enzymes, matrix metalloproteinases and their inhibitors, and tissue inhibitors of metalloproteinases and are thus able to remodel the extracellular matrix. Myofibroblasts and their microenvironment form a network that evolves during tissue repair. This network has reciprocal actions affecting cell differentiation, cell proliferation, cell quiescence, or apoptosis and has actions on growth factor bioavailability by binding, sequestration, and activation. Mechanical forces also play a role in regulating the myofibroblast phenotype as cells are subjected to mechanical stress and mechanical signaling is activated. Innervation is also involved in both skin repair processes and differentiation of myofibroblasts. In pathological situations, for example, in excessive scarring, the dialogue between myofibroblasts and their microenvironment can be altered or disrupted, leading to defects in tissue repair or to pathological scarring, such as that seen in hypertrophic scars. Better understanding of the intimate dialogue between myofibroblasts and their local microenvironment is needed and will be important in aiding the identification of new therapeutic targets and discovery of new drugs to treat or prevent aberrant tissue repair and scarring.
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Thiemermann, Christoph. "Combined Use of Nitric Oxide and Nitric Oxide Synthase Inhibitors as a Possible Therapeutic Approach." In Nitric Oxide in Pulmonary Processes: Role in Physiology and Pathophysiology of Lung Disease, 209–25. Basel: Birkhäuser Basel, 2000. http://dx.doi.org/10.1007/978-3-0348-8474-7_12.

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Jung, Jin G., and Anne Le. "Metabolism of Immune Cells in the Tumor Microenvironment." In The Heterogeneity of Cancer Metabolism, 173–85. Cham: Springer International Publishing, 2021. http://dx.doi.org/10.1007/978-3-030-65768-0_13.

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AbstractThe tumor microenvironment (TME) is a complex biological structure surrounding tumor cells and includes blood vessels, immune cells, fibroblasts, adipocytes, and extracellular matrix (ECM) [1, 2]. These heterogeneous surrounding structures provide nutrients, metabolites, and signaling molecules to provide a cancer-friendly environment. The metabolic interplay between immune cells and cancer cells in the TME is a key feature not only for understanding tumor biology but also for discovering cancer cells’ vulnerability. As cancer immunotherapy to treat cancer patients and the use of metabolomics technologies become more and more common [3], the importance of the interplay between cancer cells and immune cells in the TME is emerging with respect to not only cell-to-cell interactions but also metabolic pathways. This interaction between immune cells and cancer cells is a complex and dynamic process in which immune cells act as a determinant factor of cancer cells’ fate and vice versa. In this chapter, we provide an overview of the metabolic interplay between immune cells and cancer cells and discuss the therapeutic opportunities as a result of this interplay in order to define targets for cancer treatment. It is important to understand and identify therapeutic targets that interrupt this cancerpromoting relationship between cancer cells and the surrounding immune cells, allowing for maximum efficacy of immune checkpoint inhibitors as well as other genetic and cellular therapies.
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"Inhibitors of Matrix Metalloproteinases: Design, Structure and Therapeutic Applications." In Frontiers in Medicinal Chemistry - (Volume 1), edited by Jerry W. Skiles, Nina C. Gonnella, and Arco Y. Jeng, 29–75. BENTHAM SCIENCE PUBLISHERS, 2012. http://dx.doi.org/10.2174/978160805204210401010029.

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COURTNEY, M., S. JALLAT, D. CARVALLO, R. G. CRYSTAL, M. SCHAPIRA, and C. ROITSCH. "ANTIPROTEASE ENGINEERING: NEW PROTEASE INHIBITORS FOR THERAPEUTIC USE." In Protides of the Biological Fluids, 493–95. Elsevier, 1987. http://dx.doi.org/10.1016/b978-0-08-035588-7.50113-8.

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Nevzorova, Vera, Tatiana Brodskaya, and Eugeny Gilifanov. "Smoking and COPD: Endothelium-Related and Neuro-mediated Emphysema Mechanisms." In Update in Respiratory Diseases. IntechOpen, 2020. http://dx.doi.org/10.5772/intechopen.85927.

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This chapter describes endothelium-related and neuro-mediated mechanisms of emphysema development in chronic obstructive pulmonary disease (COPD) and smoking on the basis of previously completed studies, literature data, and own researches. As components of neurogenic inflammation in the processes of tissue remodeling in emphysema, we describe the distribution and activity of the substance P, neurokinin-1 and its receptor, tissue metalloproteinases and their tissue inhibitors in the lungs during the entire experimental period, the modeling of COPD in rats with a smoking model. We also analyzed the content of neurokinin system markers, the localization, and markers of tissue metalloproteinases in human lung tissue structures. We have confidence that there is a special morphofunctional continuum of development of lower respiratory tract remodeling in response to chronic exposure to tobacco smoke and the development of inflammation in COPD. New data suggest that imbalance of neuro-mediated interactions, alteration of vasomotoric signaling mechanisms, secretion, mucociliary clearance, cytoprotection involving substance P-dependent components with impaired content, and development of dystopia of matrix metalloproteinases and their tissue inhibitors are involved in the initiation of morphological restructuring. Research in this direction should be continued to allow approaches to the development of preventive and therapeutic strategies for emphysema.
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Angeli, Andrea, and Claudiu T. Supuran. "Therapeutic Use of Carbonic Anhydrase Inhibitors and Their Multiple Drug Interactions." In Pharmaceutical Biocatalysis, 73–98. Jenny Stanford Publishing, 2019. http://dx.doi.org/10.1201/9780429295034-3.

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Ma, Zetong, Wenyan Fu, Changhai Lei, and Shi Hu. "Use of MET kinase inhibitors to overcome cetuximab resistance in colorectal cancer." In Novel Sensitizing Agents for Therapeutic Anti-EGFR Antibodies, 113–17. Elsevier, 2023. http://dx.doi.org/10.1016/b978-0-12-821584-5.00019-5.

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Keeling, David. "Therapeutic anticoagulation." In Oxford Textbook of Medicine, edited by Jeremy Dwight, 3729–34. Oxford University Press, 2020. http://dx.doi.org/10.1093/med/9780198746690.003.0376.

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The main indications for therapeutic anticoagulation are venous thromboembolism, deep vein thrombosis, and pulmonary embolism, and the prevention of stroke in patients with atrial fibrillation or mechanical heart valves. Low-molecular-weight heparins have largely replaced unfractionated heparin in its treatment. Their much more predictable anticoagulant response combined with high bioavailability after subcutaneous injection means that the dose can be calculated by body weight and given subcutaneously without any monitoring or dose adjustment. Their widespread use resulted in most patients with deep vein thrombosis being managed as outpatients, and this is also increasingly the case for uncomplicated pulmonary embolism. Oral direct inhibitors of anticoagulation that specifically target thrombin or factor Xa are increasingly used to treat acute venous thromboembolism and for stroke prevention in atrial fibrillation.
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Alayande, Kazeem A., Abdulwakeel A. Ajao, and Mariam O. Oyedeji- Amusa. "Bioactive Compounds as Therapeutic Intervention in Bacterial Infections." In Therapeutic Use of Plant Secondary Metabolites, 139–60. BENTHAM SCIENCE PUBLISHERS, 2022. http://dx.doi.org/10.2174/9789815050622122010009.

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This study highlights the significance of drug resistance towards difficultiesin the treatment of infectious diseases, the essence of bioactive compounds intherapeutic intervention, and the unique approach employed by bioactive compoundsaway from conventional synthetic drugs. Literature was gathered from different onlinedatabases to retrieve the required information. Bacterial resistance to antibiotics is amajor concern that threatens clinical efforts in treating bacterial infections. This hasgrossly reduced clinical success on previously curable infections and/or sometimesresults in a prolonged hospital stay. Antibiotics provide protection and remedy againstinfectious diseases. But the emergence of multi-drug resistance strains has inflicteduntold loss of effectiveness on virtually every conventional antibiotic. Hence, scientificcommunities are propelled into seeking alternative therapies in a bid to mitigate theoverwhelming consequence on public health. Bioactive molecules are importantsources of newly derived therapeutic agents. They have minimal likelihood of inducingunintended immune reactions, reduced level of toxicity; are structurally diverse innature, exhibit broad-spectrum therapeutic effects. Bioactive molecules are commonlypresent in small amounts in plant-based foods; and provide health benefits in additionto the basic nutritional values expected in foods. Several plant-based bioactiveprinciples serve as inhibitors for drug resistance in order to enhance the effectivedelivery of the antibacterial compounds. Meat products are a good source of non-plantbioactive molecules, which are expressed in the form of peptides, vitamins, mineralsand fatty acids. Other important sources include endophytic bacteria, endophytic fungi,probiotic bacteria, actinomycetes and marine organisms. Natural products are relatively safe when compared to their synthetic counterparts. As newly manufactured potentantibiotics become increasingly unavailable and/or unaffordable, bioactive compoundspresent viable alternatives. They are readily available and are derived from inexpensiveraw materials via cheap technology.
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Conference papers on the topic "Metalloproteinases Inhibitors Therapeutic use"

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Meng, Wilson S., Jeffrey R. Kovacs, and Ellen S. Gawalt. "The Use of Non-Viral Nucleic Acids Carriers for the Modulation of Leukocytes." In ASME 2008 Conference on Smart Materials, Adaptive Structures and Intelligent Systems. ASMEDC, 2008. http://dx.doi.org/10.1115/smasis2008-348.

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Induction of drug-free permanent organ accommodation is the ultimate goal of transplant therapy. Current pharmacological agents, however, are non-specific in their actions and generally do not confer immunological tolerance. Inhibitors of T cell receptor signaling (tacrolimus and cyclosporine A) represent the mainstay in transplant management. These agents exert their therapeutic effects by dampening the activities of all T cells. Chronic exposure to these agents increases the risk of developing opportunistic infections and malignancies. Given that more than 20,000 Americans undergo organ transplantations each year, there is an urgent need to develop specific therapies to mitigate graft rejection and create conditions conducive for long-term transplant accommodation.
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Yalcin, Huseyin, Hissa Al-Thani, and Samar Shurbaji. "Development and In Vivo Testing of Smart Nanoparticles for Enhanced Anti-Cancer Activity and Reduced Cardiotoxicity Associated with Tyrosine Kinase Inhibitors." In Qatar University Annual Research Forum & Exhibition. Qatar University Press, 2021. http://dx.doi.org/10.29117/quarfe.2021.0088.

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Tyrosine kinase inhibitors (TKIs) are new generation of anti-cancer drugs with very high efficiency against cancer cells. However, TKIs are associated with severe cardiotoxicity limiting their clinical benefits. One TKI that has been developed recently but not explored much is Ponatinib. The use of nanoparticles as a better therapeutic agent to deliver anti-cancer drugs and reduce their cardiotoxicity has been recently considered. In this study, PLGA-PEG-PLGA nanoparticles were synthesized to deliver Ponatinib while reducing its cardiotoxicity for treatment of chronic myeloid leukemia. Shape, size, surface charge and drug uptake ability of these nanoparticles were assessed using transmission electron microscopy (TEM), ZetaSIZER NANO and high-performance liquid chromatography (HPLC). Cardiotoxicity of Ponatinib, unloaded and loaded PLGA-PEG-PLGA nanoparticles were studied on zebrafish model through measuring the survival rate and cardiac function parameters, to optimize efficient drug concentrations in an in vivo setting. These particles were tested on zebrafish cancer xenograft model in which, K562 cell line, was transplanted into zebrafish embryos. We showed that, at an optimal concentration (0.0025mg/ml), Ponatinib loaded PLGA-PEG-PLGA particles are non-toxic/non-cardio-toxic and are very efficient against cancer growth and metastasis. Zebrafish is a good animal model for investigating the cardiotoxicity associated with the anti-cancer drugs such as TKIs, to determine the optimum concentration of smart nanoparticles with the least side effects and to generate xenograft model of several cancer types. Also, PLGA-PEG-PLGA NPs could be good candidate for CML treatment, but their cellular internalization should be enhanced. This could be achieved by coating and labeling the surface of PLGA-PEG-PLGA NPs with specific ligands that are unique to CML cells.
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Arora, Rahul D. "Definition, etiopathogenesis, management and role of flouroquinolone prophylaxis in prevention of spontaneous bacterial peritonitis complicating malignant ascites." In 16th Annual International Conference RGCON. Thieme Medical and Scientific Publishers Private Ltd., 2016. http://dx.doi.org/10.1055/s-0039-1685345.

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Background: Malignancy related ascites encompasses multiple etiologies which include peritoneal carcinomatosis, hepatic synthetic dysfunction due to parenchymal involvement by the tumour, transcoeloemic metastasis and chylous ascites due to lymphatic obstruction. Primary Cancer type, liver metastasis and serum albumin have been listed as independent prognostic markers in malignant ascites. Spontaneous Bacterial Peritonitis is usually seen as a complication of decompensated chronic liver disease due to translocation of bacteria or haematogenous dissemination from a distant focus of infection. The combination of a positive peritoneal fluid culture and an ascitic fluid neutrophil count >250 cells/mm3 and no evidence of intra-abdominal source of infection; or 2) culture negative neutrocytic ascites: the combination of negative peritoneal fluid bacterial culture and neutrophil count >500 cells/mm3, without antibiotics within 7 days with no obvious source of infection are used to define spontaneous bacterialperitonitis. Ciprofloxacin prophylaxis has been proposed as a prophylaxis to reduce the incidence and prevent the recurrence of spontaneous bacterial peritonitis. Materials and Methods: A web search of indexed literature was carried out articles containing information on spontaneous bacterial peritonitis in the setting of malignancy or malignancy related ascites or malignant ascites. Articles that carried relevant information about etiopathogenesis, management and translational research in the context of malignant ascites were also included. Results: A total of 32 articles were analysed and about half of them included in the discussion to answer the research question. Discussion: Inflammatory cytokines released by tumor and immune cells compromise the mesothelial cell layer that lines the peritoneal cavity, exposing the underlying extracellular matrix to which cancer cells readily attach leading to formation of spheroids which imparts resistance to anoikis, apoptosis and chemotherapeutics leading to efficient feed forward progressive cycle of seeding and growth of peritoneal metastasis. Intraperitoneal metastasis can cause peritoneal dysfunction, adhesions and malignant ascites. Epithelial mesenchymal transistion and myofibroblastic transformation occur in the mesothelial cells in response to pathological stimuli. Vascular endothelial growth factor is an important mitogen for endothelial cells and plays an important role in increasing capillary vascular permeability. In preclinical studies systemic administration of VEGF Trap which acts as a decoy receptor for VEGF has shown to decrease the formation of ascites fluid and prevent tumour dissemination. Epithelial ovarian cancer cells have developed various mechanisms to evade immune surveillance like development of surface microvesicles which contain CD 95 ligand leading to apoptosis of immune cells. Higher levels of osteoproteogerin, IL 10 and leptin in the ascitic fluid have been associated with a poor prognosis in malignant ascites. Tethered bowel sign and presence of fluid in the omental bursa on CT have been shown to distinguish between malignant ascites and Cirrhotic ascites with accuracy. Immunological approaches to management of malignant ascites include use of intraperitoneal triamcinolone, interferon, long acting synthetic corticosteroids and the trifoliate antibody catumaxomab. VEGF Inhihibitors like octreotide and long acting depot preparations of lanreotide have also been shown to be feasible therapeutic options. Anti androgenic agents and PARP inhibitors have also been proposed as management options. Spontaneous bacterial peritonitis in the setting of malignancy in the absence of hepatic dysfunction has been reported to have a poorer prognosis than SBP in the setting of decompensated liver disease. Monomicrobial and polymicrobial bacterascites have been proposed in the absence of an elevated neutrophil ascitic fluid count that does not meet the diagnostic criteria. Extensive liver metastasis where the diseased liver can be expected to behave like a cirrhotic liver and gastrointestinal bleeding (on the basis of an isolated case report) have been considered as risk factors for the development of SBP in malignant ascites. In a case series of 8 patients with malignancy related ascites Patients with total ascitic fluid concentration of less than 1 gm per litre were found to be at risk for Spontaneous bacterial peritonitis and warrant flouroquinolone prophylaxis. Conclusion: Spontaneous Bacterial Peritonitis complicating malignant ascites is questionable entity. Good quality Audits and Randomised control trials are warranted to in this domain to enable the definition of incidence, antecedent complications, management and prophylaxis to ensure applicability of translational research to the clinical domain.
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