The cost of cosmetic surgery tourism complications to the NHS: A retrospective analysis.

INTRODUCTION: Medical tourism refers to the process of patients travelling outside of their native country to undergo elective surgical procedures and is a rapidly expanding healthcare phenomenon [1-3]. Whilst a multitude of established Private Healthcare Providers (PHPs) offer cosmetic surgical procedures within the United Kingdom (UK), a growing number of patients are opting to travel outside of the UK to undergo cosmetic surgery. AIM: To assess the number of patients presenting to the Canniesburn Plastic Surgery Unit, with cosmetic surgery tourism complications, from outside of the UK, and the associated costs to NHS Scotland over a five-year period. METHODS: A retrospective case review of a prospectively maintained trauma database, which records all acute referrals, was undertaken analysing patients referred from January 1st 2019 to December 31st 2023 inclusive. RESULTS: 81 patients presented over five years with complications of cosmetic surgery tourism. The most common presenting complaints were wound dehiscence (49.4%) or wound infection (24.7%). The total cost to NHS Scotland was £755,559.68 with an average of £9327.90 per patient. CONCLUSION: This is the largest single centre cohort of cosmetic surgery tourism complications reported within the NHS to date; with rates on the rise, demand grows for increased patient information regarding healthcare tourism risks, a national consensus on the extent of NHS management and urgent international collaboration with policymakers is required to address this issue across borders.

Methods of Cell Propulsion through the Local Stroma in Breast Cancer.

In the normal breast, cellular structures change cyclically in response to ovarian hormones. Cell proliferation, apoptosis, invasion, and differentiation are integral processes that are precisely regulated. Normal epithelial cells depend on the formation of intercellular adhesion contacts to form a continuous sheet of stratifying cell layers that are attached to one and other horizontally and vertically. Cells migrate by extending membrane protrusions to explore the extracellular space locating their targets in a chemotactic manner. The formation of cell protrusions is driven by the assembly of actin filaments at the leading edge. Reorganisation is regulated by a highly integrated signalling cascade that transduces extracellular stimuli to the actin filaments. This signalling cascade is governed by GTPases which act as molecular switches leading to actin polymerisation and the formation of filopodia and lamellipodia. This process is linked to downstream molecules known collectively as WASP proteins, which, in the presence of cortactin, form a complex leading to nucleation and formation of branched filaments. In breast cancer, the cortactin is over expressed leading to increased cellular motility and invasiveness. This hugely complex and integrated signalling cascade transduces extracellular stimuli. There are multiple genes related to cell motility which are dysregulated in human breast cancers.

The Complex Interaction of Matrix Metalloproteinases in the Migration of Cancer Cells through Breast Tissue Stroma.

Breast cancer mortality is directly linked to metastatic spread. The metastatic cell must exhibit a complex phenotype that includes the capacity to escape from the primary tumour mass, invade the surrounding normal tissue, and penetrate into the circulation before proliferating in the parenchyma of distant organs to produce a metastasis. In the normal breast, cellular structures change cyclically in response to ovarian hormones leading to regulated cell proliferation and apoptosis. Matrix metalloproteinases (MMPs) are a family of zinc dependent endopeptidases. Their primary function is degradation of proteins in the extracellular matrix to allow ductal progression through the basement membrane. A complex balance between matrix metalloproteinases and their inhibitors regulate these changes. These proteinases interact with cytokines, growth factors, and tumour necrosis factors to stimulate branching morphologies in normal breast tissues. In breast cancer this process is disrupted facilitating tumour progression and metastasis and inhibiting apoptosis increasing the life of the metastatic cells. This paper highlights the role of matrix metalloproteinases in cell progression through the breast stroma and reviews the complex relationships between the different proteinases and their inhibitors in relation to breast cancer cells as they metastasise.

Systems biology of human atherosclerosis.

Systems biology describes a holistic and integrative approach to understand physiology and pathology. The "omic" disciplines include genomics, transcriptomics, proteomics, and metabolic profiling (metabonomics and metabolomics). By adopting a stance, which is opposing (yet complimentary) to conventional research techniques, systems biology offers an overview by assessing the "net" biological effect imposed by a disease or nondisease state. There are a number of different organizational levels to be understood, from DNA to protein, metabolites, cells, organs and organisms, even beyond this to an organism's context. Systems biology relies on the existence of "nodes" and "edges." Nodes are the constituent part of the system being studied (eg, proteins in the proteome), while the edges are the way these constituents interact. In future, it will be increasingly important to collaborate, collating data from multiple studies to improve data sets, making them freely available and undertaking integrative analyses.

Review of trans-atlantic cardiovascular best medical therapy guidelines - recommendations for asymptomatic carotid atherosclerosis.

The annual rate of ipsilateral stroke associated with asymptomatic carotid stenosis has fallen from 2-4% to <1% in the last 20 years due to improvements in medical therapy. The fundamental benefits of this are relevant to whether patients undergo revascularisation or not. We aimed to evaluate existing international guidelines for the management of carotid stenosis, identifying important similarities and differences. The websites of the American Heart Association, Society for Vascular Surgery, European Society for Cardiology, European Society for Vascular Surgery, British Cardiovascular Society and UK Vascular Society were searched for guidelines relating to primary prevention for asymptomatic atherosclerotic carotid disease in September 2011 and independently reviewed by 2 authors. The following guidelines were identified and compared: The Joint British Societies 2nd (JBS2) 2005 guideline, the 4th European Society for Cardiology (ESC) 2007 guideline, the joint American Heart Association/Society for Vascular Surgery (AHA/SVS) guideline 2011 and subsequent 2011 SVS update, the American Heart Association (AHA) prevention of stroke guideline 2010, the AHA secondary prevention for atherosclerotic coronary and vascular disease 2011 update, and the European Society for Vascular Surgery (ESVS) Section A carotid guideline. There was no UK guidance from its vascular society. Important differences were evident in methods of risk assessment, treatment targets for blood pressure and low density lipoprotein cholesterol, and the use of anti-platelet agents. These differences are highlighted in 2 case scenarios. There is now clear, evidence based guidance from British, European and US cardiovascular bodies regarding optimal targets for risk factor modification. These can be adopted as standard operating procedure for clinical practice and the medical arms of carotid interventional trials. In the future imaging biomarkers may help provide an understanding of the risk of an individual carotid lesion to help guide therapy.

Periprocedural outcomes after surgical revascularization and stenting for postradiotherapy carotid stenosis.

BACKGROUND: Treatment of head and neck malignancy commonly involves radiotherapy, which is associated with the development of carotid artery stenosis. There is little evidence to guide clinicians on how to intervene in significant postradiotherapy carotid stenosis. This systematic review collated data pertaining to perioperative outcomes of carotid artery surgery and carotid stenting in postradiotherapy carotid stenosis to aid the clinical decision-making process. METHODS: A systematic review of the literature, adhering to the Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) 2009 guidelines, was performed. We screened 575 articles related to carotid artery surgery or stenting in postradiotherapy carotid stenosis, from which 21 studies were included for quantitative analysis. The primary outcome was stroke or death ≤ 30 days of the procedure. Secondary outcomes included cranial nerve injury, restenosis, stroke, and death at >30 days. RESULTS: Nine publications recorded 211 surgical procedures in 179 patients. In symptomatic patients, the 30-day mortality rate was 2.6% and the stroke or death rate was 2.7%. In asymptomatic patients, the 30-day mortality rate was 0% and the stroke or death rate was 1.1%. Permanent cranial nerve palsy was experienced by 0.6% of patients. Twelve publications recorded 510 carotid artery stenting procedures in 482 patients. In symptomatic patients, the 30-day mortality rate was 5.1%, and the stroke or death rate was 5.1%. In asymptomatic patients, the 30-day mortality rate was 1.4%, and the stroke or death rate was 2.1%. There was no statistically significant difference in 30-day stroke or death rate between surgical revascularization and carotid artery stenting in all (odds ratio [OR], 0.54; 95% confidence interval [CI] 0.17-1.70; P = .43), symptomatic (OR, 0.52; 95% CI, 0.14-1.98; P = .38), or asymptomatic patients (OR, 0.55; 95% CI, 0.06-5.42; P = .99). CONCLUSIONS: The published outcomes from high-volume centers demonstrate that surgical revascularization and stenting are both technically feasible in postradiotherapy carotid stenosis and have similar safety profiles to nonirradiated necks. Radiation should therefore not be considered a contraindication to surgical intervention.

The utility of collaborative biobanks for cardiovascular research.

Differences between animal and human atherosclerosis have led to the requirement for clinical data, imaging information and biological material from large numbers of patients and healthy persons. Where such "biobanks" exist, they have been fruitful sources for genomewide association, diagnostic accuracy, ethnicity, and risk stratification cohort studies. In addition once established, they attract funding for future projects. Biobanks require a network of medical contributors, secure storage facilities, bioinformatics expertise, database managers, and ethical working practices to function optimally. There is the opportunity for collaboration between individual biobanks to further amplify the advantages afforded.