Alan John Nimmo

Prof. Dr. Alan John Nimmo

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Research Focus & Metrics

Academic Career Length

25Years (2002-Present)

(Calculated once Scilit publication data is synced: current year − year of first publication + 1)

Representative Publications

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22 December 2020 in Dentistry Journal
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Journal Article
Open access
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ASAmar Sholapurkar
Amar Sholapurkar
Dileep SharmaDileep Sharma
Dileep Sharma
BGBeverley Glass
Beverley Glass
Catherine M. MillerCatherine M. Miller
Catherine M. Miller
ANAlan John Nimmo
Alan John Nimmo
EJErnest A Jennings
Ernest A Jennings
This review sheds light on the recent published scientific evidence relating to the use of professionally delivered local antimicrobial agents (LA’s). The review also analyses drug delivery systems available to date and provides an update on the latest scientific evidence about the benefits, limitations, and clinical results obtained by use of local drugs in the treatment of periodontal disease. The search strategy revealed randomized controlled trials (RCTs) that compared the efficacy of adjunctive LA’s to mechanical therapy alone. Based on the available evidence gathered from this review, we can infer that the use of local antimicrobial agents in conjunction to scaling and root debridement (SRD) delivers significant benefits in periodontal therapy and it is a useful aid, avoiding many of the side effects that systemic antibiotic therapy may involve. Local drug delivery (LDD) is an efficient and effective means of delivering drugs based on the evidence presented in the review. The authors of this review would suggest the use of local antimicrobials in cases of localized periodontitis or individual areas that do not respond to the usual mechanical therapy alone. This review summarizes the current use of local drug delivery in periodontal management ensuring that the general practitioners are able to choose an appropriate local antimicrobial.

3 July 2002 in Clinical and Experimental Pharmacology and Physiology
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Journal Article
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ANAlan John Nimmo
Alan John Nimmo
JCJill R Carstairs
Jill R Carstairs
SPSanjay K Patole
Sanjay K Patole
JWJohn Whitehall
John Whitehall
KDKate Davidson
Kate Davidson
RVRobert Vink
Robert Vink


Verified
Journal Article
Open access
PDF file
ANAlan John Nimmo
Alan John Nimmo
AYAlexander Younsi
Alexander Younsi
Traumatic brain injuries (TBI) represent a leading cause of morbidity and mortality globally. Whilst clinical care has significantly improved in recent years, there is still significant scope to improve patient outcomes, particularly in relation to quality of life. However, there is a window of opportunity for clinical intervention, since most of the mortality and morbidity is associated with secondary injury processes that arise after the initial trauma. In the brain, as with any tissue, inflammation plays an important role in the response to injury. However, particularly with severe injuries, an excessive inflammatory response can have detrimental effects. Following TBI, inflammation can lead to the development of cerebral oedema and a rise in intracranial pressure. Without effective control, these processes can rapidly lead to patient deterioration. This narrative review focusses on the role of inflammation in TBI in order to examine the strategies that may help improve patient outcomes. Whilst there is clearly a relationship between the development of cerebral oedema, rising intracranial pressure (ICP), and poor patient prognosis, there are also discrepancies in terms of their impact on patient outcomes. In addition to causing a rise in ICP, this review examines in what other ways inflammation and the development of cerebral oedema may contribute to the injury process. The potential for these factors to impact upon microvascular function and reduce cerebral tissue perfusion and oxygenation is explored. In addition, the impact of TBI on glymphatic function is discussed. Following an evaluation of the potential injury processes, the scope for intervention and the development of novel therapeutic approaches is explored.

29 October 2019 in Australian Dental Journal
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Journal Article
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AKAHSEN KHAN
AHSEN KHAN
AGAnkit Goyal
Ankit Goyal
VSVidhi Somaiya
Vidhi Somaiya
ARAshwin Rathesh
Ashwin Rathesh
JSJathuran Sathiyamoorthy
Jathuran Sathiyamoorthy
ANAlan John Nimmo
Alan John Nimmo

26 September 2019 in Clinical & Experimental Metastasis
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Journal Article
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MEMoustafa Elhousiny
Moustafa Elhousiny
KMKate Miller
Kate Miller
AAAnura Ariyawadana
Anura Ariyawadana
ANAlan John Nimmo
Alan John Nimmo
Metastasis, whether regional or distant, remains the main cause of morbidity and recurrence in oral cancer. The accumulating evidence suggests that inflammatory mediators are strong drivers for cancer progression and spread. However, the precise role of these inflammatory mediators in mediating specific metastatic stage is poorly understood due to lack of integration/validation of experimental research data and the clinical trials, i.e., the data produced from research is not translated to clinical therapeutic targets. This, in turn, results in the lack of developing reliable biomarker that can be used for accurate diagnosis/prognosis of the tumour spread. We have performed a systematic review to assess the role of inflammatory mediators as potential markers for diagnosis/prognosis of oral squamous cell carcinoma (OSCC) metastasis. We carried out a systematic search the PubMed, Web of Science, Embase and Scopus databases under the guidelines for Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) and Australian National Health and Medical Research Council (NHMRC). Articles were divided into two groups; experimental (in-vivo) and clinical studies. The REporting recommendations for tumour MARKer prognostic studies Scale (REMARK) was used to assess the quality of the studies for the clinical search while Animal research: Reporting In-vivo experiments (ARRIVE) guidelines were used to assess the quality of the animal studies. Sixteen articles in the clinical group and four articles in the experimental group were included in the final review. We identified nine inflammatory mediators; CXCR4, CXCL12 (SDF-1), CCR7, IL-6, IL-18, CCL20 (MIP-3), CXCL1 (GRO-1), CCL3, CXCR2. This panel of inflammatory mediators can provide a framework for hypothesis testing of the potential value of these mediators in metastatic prognosis. We recommend carrying a large cohort study with data pooling for adequate assessment and testing of the inflammatory panel of mediators.