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Inflammopharmacology — Template for authors

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Guideline source

Categories	Rank	Trend in last 3 yrs
Pharmacology (medical)	#47 of 246	up by 25 ranks
Pharmacology	#76 of 297	up by 40 ranks
Immunology	#83 of 202	up by 27 ranks

Journal quality:

High

Last 4 years overview: 417 Published Papers | 2556 Citations

Indexed in: Scopus

Last updated: 01/07/2020

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General info

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Journal Performance & Insights

CiteRatio

SCImago Journal Rank (SJR)

Source Normalized Impact per Paper (SNIP)

A measure of average citations received per peer-reviewed paper published in the journal.

Measures weighted citations received by the journal. Citation weighting depends on the categories and prestige of the citing journal.

Measures actual citations received relative to citations expected for the journal's category.

6.1

39% from 2019

CiteRatio for Inflammopharmacology from 2016 - 2020
Year	Value
2020	6.1
2019	4.4
2018	3.8
2017	4.4
2016	5.0

Graph view

0.945

30% from 2019

SJR for Inflammopharmacology from 2016 - 2020
Year	Value
2020	0.945
2019	0.729
2018	0.894
2017	0.925
2016	0.941

Graph view

1.303

22% from 2019

SNIP for Inflammopharmacology from 2016 - 2020
Year	Value
2020	1.303
2019	1.064
2018	1.147
2017	1.223
2016	1.159

Graph view

Insights

CiteRatio of this journal has increased by 39% in last years.
This journal’s CiteRatio is in the top 10 percentile category.

Insights

SJR of this journal has increased by 30% in last years.
This journal’s SJR is in the top 10 percentile category.

Insights

SNIP of this journal has increased by 22% in last years.
This journal’s SNIP is in the top 10 percentile category.

Inflammopharmacology

Guideline source: View

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Springer

Inflammopharmacology

Acute and chronic inflammatory processes underlie a vast number of diseases. These processes involve production of many inflammatory mediators, which are formed from or interact with a wide range of cells, including those of the immune system, to cause various responses at specific sites in the body. This presents challenges for drug treatment of these conditions and for the effectiveness of conventional agents such as non-steroidal anti-inflammatory drugs (NSAIDs), corticosteroids, disease-modifying anti-rheumatic drugs (DMARDs), anti-cytokine and other biologic agents, as well as natural products (or nutraceuticals). The use of many of these agents is often limited by (a) the agents’ unspecific actions or limited potency at their therapeutic targets, (b) their poor pharmacokinetic properties leading to poor bioavailability of the active agents, and (c) their varying array of serious and non-serious side-effects and adverse drug reactions. Broadly speaking, Inflammopharmacology aims to publish high quality papers addressing these key problems and directed towards “advancing research into new medicines” as well as new approaches to development of safer and more effective, site-specific anti-inflammatory agents. Read Less

Pharmacology (medical)

Immunology

Medicine

Last updated on	01 Jul 2020
ISSN	0925-4692
Impact Factor	Medium - 0.825
Open Access	No
Sherpa RoMEO Archiving Policy	Green
Plagiarism Check	Available via Turnitin
Endnote Style	Download Available
Bibliography Name	SPBASIC
Citation Type	Author Year (Blonder et al, 1982)
Bibliography Example	Beenakker CWJ (2006) Specular andreev reflection in graphene. Phys Rev Lett 97(6):067,007, URL 10.1103/PhysRevLett.97.067007

Top papers written in this journal

Journal Article • DOI: 10.1007/S10787-007-0013-X •

Role of nitric oxide in inflammatory diseases

Jagdish N. Sharma¹, A. Al-Omran¹, •

01 Dec 2007 - Inflammopharmacology

Abstract:

Nitric oxide (NO) is a signaling molecule that plays a key role in the pathogenesis of inflammation. It gives an anti-inflammatory effect under normal physiological conditions. On the other hand, NO is considered as a pro-inflammatory mediator that induces inflammation due to over production in abnormal situations. NO is synt... Nitric oxide (NO) is a signaling molecule that plays a key role in the pathogenesis of inflammation. It gives an anti-inflammatory effect under normal physiological conditions. On the other hand, NO is considered as a pro-inflammatory mediator that induces inflammation due to over production in abnormal situations. NO is synthesized and released into the endothelial cells by the help of NOSs that convert arginine into citrulline producing NO in the process. Oxygen and NADPH are necessary co-factors in such conversion. NO is believed to induce vasodilatation in cardiovascular system and furthermore, it involves in immune responses by cytokine-activated macrophages, which release NO in high concentrations. In addition, NO is a potent neurotransmitter at the neuron synapses and contributes to the regulation of apoptosis. NO is involved in the pathogenesis of inflammatory disorders of the joint, gut and lungs. Therefore, NO inhibitors represent important therapeutic advance in the management of inflammatory diseases. Selective NO biosynthesis inhibitors and synthetic arginine analogues are proved to be used for the treatment of NO-induced inflammation. Finally, the undesired effects of NO are due to its impaired production, including in short: vasoconstriction, inflammation and tissue damage. read more

Topics:

Inflammation (53%)53% related to the paper, Citrulline (53%)53% related to the paper, Nitric oxide (53%)53% related to the paper,

900 Citations

Journal Article • DOI: 10.1007/S10787-013-0172-X •

The modern pharmacology of paracetamol: therapeutic actions, mechanism of action, metabolism, toxicity and recent pharmacological findings

Garry G. Graham¹, Michael J. Davies², •

30 May 2013 - Inflammopharmacology

Abstract:

Paracetamol is used worldwide for its analgesic and antipyretic actions. It has a spectrum of action similar to that of NSAIDs and resembles particularly the COX-2 selective inhibitors. Paracetamol is, on average, a weaker analgesic than NSAIDs or COX-2 selective inhibitors but is often preferred because of its better toleran... Paracetamol is used worldwide for its analgesic and antipyretic actions. It has a spectrum of action similar to that of NSAIDs and resembles particularly the COX-2 selective inhibitors. Paracetamol is, on average, a weaker analgesic than NSAIDs or COX-2 selective inhibitors but is often preferred because of its better tolerance. Despite the similarities to NSAIDs, the mode of action of paracetamol has been uncertain, but it is now generally accepted that it inhibits COX-1 and COX-2 through metabolism by the peroxidase function of these isoenzymes. This results in inhibition of phenoxyl radical formation from a critical tyrosine residue essential for the cyclooxygenase activity of COX-1 and COX-2 and prostaglandin (PG) synthesis. Paracetamol shows selectivity for inhibition of the synthesis of PGs and related factors when low levels of arachidonic acid and peroxides are available but conversely, it has little activity at substantial levels of arachidonic acid and peroxides. The result is that paracetamol does not suppress the severe inflammation of rheumatoid arthritis and acute gout but does inhibit the lesser inflammation resulting from extraction of teeth and is also active in a variety of inflammatory tests in experimental animals. Paracetamol often appears to have COX-2 selectivity. The apparent COX-2 selectivity of action of paracetamol is shown by its poor anti-platelet activity and good gastrointestinal tolerance. Unlike both non-selective NSAIDs and selective COX-2 inhibitors, paracetamol inhibits other peroxidase enzymes including myeloperoxidase. Inhibition of myeloperoxidase involves paracetamol oxidation and concomitant decreased formation of halogenating oxidants (e.g. hypochlorous acid, hypobromous acid) that may be associated with multiple inflammatory pathologies including atherosclerosis and rheumatic diseases. Paracetamol may, therefore, slow the development of these diseases. Paracetamol, NSAIDs and selective COX-2 inhibitors all have central and peripheral effects. As is the case with the NSAIDs, including the selective COX-2 inhibitors, the analgesic effects of paracetamol are reduced by inhibitors of many endogenous neurotransmitter systems including serotonergic, opioid and cannabinoid systems. There is considerable debate about the hepatotoxicity of therapeutic doses of paracetamol. Much of the toxicity may result from overuse of combinations of paracetamol with opioids which are widely used, particularly in USA. read more

Topics:

COX-3 (58%)58% related to the paper, Acetaminophen (57%)57% related to the paper, Analgesic (52%)52% related to the paper

447 Citations

Journal Article • DOI: 10.1007/S10787-009-0016-X •

Ibuprofen: pharmacology, efficacy and safety

Kim D. Rainsford¹ •

21 Nov 2009 - Inflammopharmacology

Abstract:

This review attempts to bring together information from a large number of recent studies on the clinical uses, safety and pharmacological properties of ibuprofen. Ibuprofen is widely used in many countries for the relief of symptoms of pain, inflammation and fever. The evidence for modes of action of ibuprofen are considered ... This review attempts to bring together information from a large number of recent studies on the clinical uses, safety and pharmacological properties of ibuprofen. Ibuprofen is widely used in many countries for the relief of symptoms of pain, inflammation and fever. The evidence for modes of action of ibuprofen are considered in relation to its actions in controlling inflammation, pain and fever, as well as the adverse effects of the drug. At low doses (800–1,200 mg day−1) which in many countries are approved for non-prescription (over-the-counter) sale ibuprofen has a good safety profile comparable with paracetamol. Its analgesic activity is linked to its anti-inflammatory effects and is related to reduction in the ex vivo production in blood of cyclo-oxygenase (COX)-1 and COX-2 derived prostanoids. Higher prescription doses (circa 1,800–2,400 mg day−1) are employed long-term for the treatment of rheumatic and other more severe musculo-skeletal conditions. Recent evidence from large-scale clinical trials with the newer coxibs, where ibuprofen was as a comparator, have confirmed earlier studies which have shown that ibuprofen has comparable therapeutic benefits with coxibs and other NSAIDs. For long-term usage (6+ months) there are greater numbers of drop-outs due to reduced effectiveness of therapy, a feature which is common with NSAIDs. Spontaneous reports of adverse events and adverse drug reactions (ADRs) in clinical trails from long-term coxib comparator studies, as well as in epidemiological studies, shows that ibuprofen has relatively low risks for gastro-intestinal (GI), hepato-renal and other, rarer, ADRs compared with other NSAIDs and coxibs. A slightly higher risk of cardiovascular (CV) events has been reported in some, but not all studies, but the risks are in general lower than with some coxibs and diclofenac. The possibility that ibuprofen may interfere with the anti-platelet effects of aspirin, though arguably of low grade or significance, has given rise to caution on its use in patients that are at risk for CV conditions that take aspirin for preventing these conditions. Paediatric use of ibuprofen is reviewed and the main results are that the drug is relatively safe and effective as a treatment of acute pain and fever. It is probably more effective than paracetamol as an antipyretic. This assessment of the safety and benefits of ibuprofen can be summarized thus: (1) Ibuprofen at OTC doses has low possibilities of serious GI events, and little prospect of developing renal and associated CV events. Ibuprofen OTC does not represent a risk for developing liver injury especially the irreversible liver damage observed with paracetamol and the occasional liver reactions from aspirin. (2) The pharmacokinetic properties of ibuprofen, especially the short plasma half-life of elimination, lack of development of pathologically related metabolites (e.g. covalent modification of liver proteins by the quinine–imine metabolite of paracetamol or irreversible acetylation of biomolecules by aspirin) are support for the view that these pharmacokinetic and notably metabolic effects of ibuprofen favour its low toxic potential. (3) The multiple actions of ibuprofen in controlling inflammation combine with moderate inhibition of COX-1 and COX-2 and low residence time of the drug in the body may account for the low GI, CV and renal risks from ibuprofen, especially at OTC doses. read more

Topics:

Antipyretic (59%)59% related to the paper, Analgesic (56%)56% related to the paper, Ibuprofen (56%)56% related to the paper,

418 Citations

Journal Article • DOI: 10.1007/S10787-015-0239-Y •

Therapy and pharmacological properties of hydroxychloroquine and chloroquine in treatment of systemic lupus erythematosus, rheumatoid arthritis and related diseases

Kim D. Rainsford¹, Ann L. Parke, •

06 Aug 2015 - Inflammopharmacology

Abstract:

This review examines the pharmacokinetics, modes of action and therapeutic properties of the anti-malarial drugs, hydroxychloroquine (HCQ) and chloroquine (CQ), in the treatment of systemic lupus erythematosus (SLE), rheumatoid arthritis (RA) and related conditions, as well as osteoarthritis (OA). Both HCQ and CQ have histor... This review examines the pharmacokinetics, modes of action and therapeutic properties of the anti-malarial drugs, hydroxychloroquine (HCQ) and chloroquine (CQ), in the treatment of systemic lupus erythematosus (SLE), rheumatoid arthritis (RA) and related conditions, as well as osteoarthritis (OA). Both HCQ and CQ have historically been employed successfully for the treatment of SLE and RA for over 70 years. HCQ has been used extensively for SLE where it has a good reputation for controlling the dermatological complications in SLE. It has also been reported to effectively control the symptoms of Sjogren’s syndrome, as well as preventing thrombosis in phospholipid antibody (aPL) syndrome. In RA and SLE, HCQ is preferred because of the lower incidence of gastrointestinal adverse reactions compared with CQ and it might have a lower risk of ocular adverse reactions. There is increasing evidence that HCQ may reduce atherosclerosis and risks of cardiovascular disease in rheumatic patients. Both HCQ and CQ have been shown to improve glycaemia and reduce the risks of type II diabetes mellitus. Although both HCQ and CQ are effective in low-moderate RA, HCQ is now preferred as part of combination therapy for more severe disease. The advantages of combination therapy are that the doses of the individual drugs may be lowered so reducing adverse reactions. Both HCQ and CQ are diastereoisomers, have basic properties and are given as the sulphate and phosphate salts. While being relatively well absorbed orally and with good bioavailability, they have long and variable plasma terminal elimination half-lives (approximately 40–60 days). This reflects their high volume of distribution, V D (HCQ 44,000L; CQ 65,000L) which extends into aqueous compartments, long mean residence time (HCQ 1300 h; CQ 900 h) and with about half the drugs (metabolites) undergoing renal clearance. The strong binding to melanin reflects the ocular injury and dermatological properties of these drugs. The consensus is that the occurrence of ocular adverse reactions can be minimised by close attention to the dose (which should be set on a body weight basis) with regular (e.g. quarterly) retinal examination. Although HCQ and CQ can pass through the placenta, the use of these drugs during pregnancy does not appear to risk harm to the baby and might be beneficial to the mother with SLE and her child by controlling the SLE disease activity, which is known to be an important factor affecting pregnancy outcome. The modes of action of HCQ and CQ in these arthritides represent somewhat of an enigma. Undoubtedly, these drugs have multiple actions related, in part, their ability to accumulate in lysosomes and autophagosomes of phagocytic cells as well as affecting MHC Class II expression and antigen presentation; actions of the production of pro-inflammatory cytokines [e.g. interleukin-1 (IL-1) tumour necrosis factor-α (TNFα)]; control of toll-like receptor-9 activation; and leucocyte generation of reactive oxygen species (ROS); i.e. antioxidant activity. The actions of these drugs on T and B cells are less clear but may depend on these leucocyte-mediated actions. Anti-malarials also protect against cytokine-mediated cartilage resorption. This and other actions may underlie the potential benefits in treating OA. The exact relationships of these various actions, mostly determined in vitro, have not been specifically defined in vivo or ex vivo in relation to clinical efficacy. HCQ and CQ have a good reputation for being effective and relatively safe treatments in SLE, mild-moderate RA and Sjogren’s syndrome. There is need for (a) more information on their mode of action in relation to the control of these diseases, (b) scope for developing formulations that have improved pharmacokinetic and therapeutic properties and safety, and (c) further exploring their use in drug combinations not only with other disease-modifying agents but also with biologics. read more

Topics:

Hydroxychloroquine (53%)53% related to the paper, Rheumatoid arthritis (51%)51% related to the paper

410 Citations

Open access • Journal Article • DOI: 10.1007/S10787-017-0309-4 •

Antioxidant and anti-inflammatory effects of zinc. Zinc-dependent NF-κB signaling

Magdalena Jarosz¹, Magdalena Olbert¹, •

12 Jan 2017 - Inflammopharmacology

Abstract:

Zinc is a nutritionally fundamental trace element, essential to the structure and function of numerous macromolecules, including enzymes regulating cellular processes and cellular signaling pathways. The mineral modulates immune response and exhibits antioxidant and anti-inflammatory activity. Zinc retards oxidative processes... Zinc is a nutritionally fundamental trace element, essential to the structure and function of numerous macromolecules, including enzymes regulating cellular processes and cellular signaling pathways. The mineral modulates immune response and exhibits antioxidant and anti-inflammatory activity. Zinc retards oxidative processes on a long-term basis by inducing the expression of metallothioneins. These metal-binding cysteine-rich proteins are responsible for maintaining zinc-related cell homeostasis and act as potent electrophilic scavengers and cytoprotective agents. Furthermore, zinc increases the activation of antioxidant proteins and enzymes, such as glutathione and catalase. On the other hand, zinc exerts its antioxidant effect via two acute mechanisms, one of which is the stabilization of protein sulfhydryls against oxidation. The second mechanism consists in antagonizing transition metal-catalyzed reactions. Zinc can exchange redox active metals, such as copper and iron, in certain binding sites and attenuate cellular site-specific oxidative injury. Studies have demonstrated that physiological reconstitution of zinc restrains immune activation, whereas zinc deficiency, in the setting of severe infection, provokes a systemic increase in NF-κB activation. In vitro studies have shown that zinc decreases NF-κB activation and its target genes, such as TNF-α and IL-1β, and increases the gene expression of A20 and PPAR-α, the two zinc finger proteins with anti-inflammatory properties. Alternative NF-κB inhibitory mechanism is initiated by the inhibition of cyclic nucleotide phosphodiesterase, whereas another presumed mechanism consists in inhibition of IκB kinase in response to infection by zinc ions that have been imported into cells by ZIP8. read more

Topics:

Zinc finger (63%)63% related to the paper, Zinc (61%)61% related to the paper, Zinc deficiency (60%)60% related to the paper,

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355 Citations

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After writing your paper autoformatting in Inflammopharmacology, you can download it in multiple formats, viz., PDF, Docx, and LaTeX.

12. Is Inflammopharmacology's impact factor high enough that I should try publishing my article there?

To be honest, the answer is no. The impact factor is one of the many elements that determine the quality of a journal. Few of these factors include review board, rejection rates, frequency of inclusion in indexes, and Eigenfactor. You need to assess all these factors before you make your final call.

13. What is Sherpa RoMEO Archiving Policy for Inflammopharmacology?

We extracted this data from Sherpa Romeo to help researchers understand the access level of this journal in accordance with the Sherpa Romeo Archiving Policy for Inflammopharmacology. The table below indicates the level of access a journal has as per Sherpa Romeo's archiving policy.

RoMEO Colour	Archiving policy
Green	Can archive pre-print and post-print or publisher's version/PDF
Blue	Can archive post-print (ie final draft post-refereeing) or publisher's version/PDF
Yellow	Can archive pre-print (ie pre-refereeing)
White	Archiving not formally supported

FYI:

Pre-prints as being the version of the paper before peer review and
Post-prints as being the version of the paper after peer-review, with revisions having been made.

14. What are the most common citation types In Inflammopharmacology?

The 5 most common citation types in order of usage for Inflammopharmacology are:.

S. No.	Citation Style Type
1.	Author Year
2.	Numbered
3.	Numbered (Superscripted)
4.	Author Year (Cited Pages)
5.	Footnote

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Yes, SciSpace provides this functionality. After signing up, you would need to import your existing references from Word or Bib file to SciSpace. Then SciSpace would allow you to download your references in Inflammopharmacology Endnote style according to Elsevier guidelines.

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Related Journals

Journal Performance & Insights

CiteRatio

SCImago Journal Rank (SJR)

Source Normalized Impact per Paper (SNIP)

6.1

0.945

1.303

Insights

Insights

Insights

Inflammopharmacology

Inflammopharmacology

Top papers written in this journal

Abstract:

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Abstract:

Topics:

Abstract:

Topics:

Abstract:

Topics:

Abstract:

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What to expect from SciSpace?

Speed and accuracy over MS Word

Plagiarism Reports via Turnitin

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Frequently asked questions

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No word template required

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Trusted by academicians

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