• Calcium alginate dressings promote healing of split skin graft donor sites.

      O'Donoghue, J M; O'Sullivan, S T; Beausang, E S; Panchal, J I; O'Shaughnessy, M; O'Connor, T P; Department of Plastic Surgery, Cork University Hospital, Wilton, Ireland. (2012-02-03)
      A prospective controlled trial was carried out to assess the healing efficacy of calcium alginate and paraffin gauze on split skin graft donor sites. Thirty patients were randomised to the calcium alginate group and 21 to the paraffin gauze group. The donor sites were assessed at 10 days post harvesting to determine if they were completely healed (100%) or not. Twenty one of the 30 patients dressed with calcium alginate were completely healed at day 10, while only 7/21 in the paraffin gauze group were healed (p < 0.05). There were two infections in the study, both occurring in the alginate group while there was no difference in dressing slippage between the two groups. Calcium alginate dressings provide a significant improvement in healing split skin graft donor sites.
    • Campylobacter ureolyticus: an emerging gastrointestinal pathogen?

      Bullman, Susan; Corcoran, Daniel; O'Leary, James; Lucey, Brigid; Byrne, Deirdre; Sleator, Roy D; Department of Biological Sciences, Cork Institute of Technology, Cork, Ireland. (Blackwell Publishing Ltd., 2011-03)
      A total of 7194 faecal samples collected over a 1-year period from patients presenting with diarrhoea were screened for Campylobacter spp. using EntericBio(®) , a multiplex-PCR system. Of 349 Campylobacter-positive samples, 23.8% were shown to be Campylobacter ureolyticus, using a combination of 16S rRNA gene analysis and highly specific primers targeting the HSP60 gene of this organism. This is, to the best of our knowledge, the first report of C. ureolyticus in the faeces of patients presenting with gastroenteritis and may suggest a role for this organism as an emerging enteric pathogen.
    • Can mean platelet component be used as an index of platelet activity in stable coronary artery disease?

      Cooke, John; Murphy, Tracy; McFadden, Eugene; O'Reilly, Mairead; Cahill, Mary R; Mid-Western Regional Hospital, Dooradoyle, Limerick, Ireland. (2009-04)
      Acute coronary syndrome is associated with intracoronary thrombosis secondary to platelet activation. Previous groups have investigated platelet activation in both stable and unstable vascular disease. Most measures of platelet activation are not routinely available or easily adaptable to large scale clinical use. Recently, measurement of the mean platelet component (MPC) has become part of the routine data provided by an automated full blood count analyser, the Advia 120. MPC measures platelet density which changes on platelet activation. Our objectives were to determine if platelet activation, as measured by MPC, is increased in patients with stable coronary artery disease (CAD) and to determine if MPC could be useful in differentiating people with stable CAD from controls on an everyday clinical basis. Three hundred and forty-five consecutive patients attending for elective coronary angiography had full blood count analysis and MPC measurement performed using an ADVIA-120 analyser. Three hundred and twenty-four were analysed in our final dataset. Two hundred and fifty-three (78%) had CAD. Patients with CAD were significantly (p<0.001) older than those without (63.8 versus 56.0 years). Results failed to demonstrate a difference (p=0.467) in MPC between patients with CAD and those with normal coronary arteries (25.8 versus 26.0). Likewise, there was no correlation between MPC and the severity of CAD (Kendall's tau b=-0.086, p=0.04). MPC is not a useful index of platelet activity in stable CAD when used in everyday clinical practice.
    • Can state or response entropy be used as a measure of sleep depth?

      Mahon, P; Greene, B R; Lynch, E M; McNamara, B; Shorten, G D; Department of Anaesthesia and Intensive Care Medicine, Cork University Hospital, and University College Cork, Cork, Ireland. rsimahon@hotmail.com (2012-02-03)
      SUMMARY: In this prospective observational study we examined the potential of the spectral entropy measures 'state' and 'response' entropy (Entropy monitor), as measures of sleep depth in 12 healthy adult subjects. Both median state and response entropy values varied significantly with sleep stage (p = 0.017 and p = 0.014 respectively; ANOVA). Median state or response entropy did not decrease significantly during the transition from awake to stage I sleep (p > 0.017). State entropy values decreased significantly between sleep stages I and II (p < 0.001). Both state and response entropy values were significantly less (40 and 45 arbitrary units respectively) in stage III (slow wave sleep) vs stage II sleep (p = 0.008). We conclude that state and response entropy values, when expressed as a function of time, may be a useful means of quantifying aspects of sleep.
    • Can you die from obstructive sleep apnoea syndrome (OSAS)?

      O'Carroll, G; Doody, E; Vaughan, C; Doherty, L (Irish Medical Journal, 2015-02)
      Studies suggest an independent association between Obstructive Sleep Apnoea Syndrome (OSAS) and cardiovascular death. The purpose of our study is to examine doctors' awareness of this association and to determine whether this correlates with recording of OSAS on death certificates. We contacted the Central Statistics Office (CSO) and obtained relevant mention of OSAS on death certificates. We surveyed doctors on their view of OSAS-related deaths, CSO data from 2008-2011 reveal two deaths with OSAS documented as a direct cause and 52 deaths with OSAS as a contributory cause. Seventy-five doctors' surveyed (41%) believe OSAS can be a direct cause of death and 177 (96%) believe OSAS can be an indirect cause of death. Only 22 (12%) had putdown OSAS as a cause of death. OSAS is seldom recorded on death certificates. This is at odds with epidemiological forecasts and contrary to an opinion poll from a selection of doctors.
    • Cancer surgery: risks and opportunities.

      Coffey, J C; Smith, M J F; Wang, J H; Bouchier-Hayes, D; Cotter, T G; Redmond, H P; Department of Surgery, Cork University Hospital, University College Cork,, National University of Ireland. calvincoffey@hotmail.com (2012-02-03)
      In the recent past, several papers have pointed to the possibility that tumour removal generates a permissive environment in which tumour growth is potentiated. This phenomenon has been coined "perioperative tumour growth" and whilst it represents a departure in terms of our attitude to the surgical process, this concept was first hinted at by Paget(1) himself. Despite this, the time interval immediately before and after cancer surgery (i.e. the perioperative period) remains an underutilised interval during which chemotherapeutic regimens are rarely implemented. Herein, we present a summarised review of the literature that supports the concept that tumour removal may potentiate the growth of residual neoplastic disease. We also outline current knowledge regarding underlying mechanisms and in this manner highlight potential therapeutic entry points. Finally, we emphasise the urgent need for trials of agents that could protect patients against the harmful host-tumour interactions that may occur during the perioperative period.
    • Candidaemia in an Irish tertiary referral hospital: epidemiology and prognostic factors.

      Boo, T W; O'reilly, B; O'leary, J; Cryan, B; Department of Microbiology, Cork University Hospital, Cork, Ireland., twboo@eircom.net (2012-02-03)
      There were two parts to this study. Part 1 evaluated the epidemiology of Candida bloodstream isolates within the Southern Health Board (SHB) of Ireland from 1992 to 2003 by retrospective surveillance of all such isolates of patients reported from SHB hospitals to our laboratory database during that period. Part 2 reviewed candidaemia cases occurring in Cork University Hospital (CUH) from 1999 to 2003 using surveillance of all positive blood culture isolates in CUH microbiology laboratory during the 5-year period. In part 1, 250 Candida bloodstream isolates were reported in the SHB over 12 years. There was a pattern of decreasing percentage of C. albicans with time. Whereas in part 2, 63 cases of candidaemia were identified in CUH from 1999 to 2003. Candida albicans constituted 50% of all isolates, while C. parapsilosis and C. glabrata accounted for 21.2% and 18.2% respectively. Average annual incidence rate was 0.48 episodes/1000 admissions and 0.70 episodes/10 000 patient-days. Vascular catheters were the commonest source of candidaemia (61.9%) followed by the urinary tract (12.7%). Risk factors included exposure to multiple antibiotics (75%); central vascular catheterization (73%); multiple colonization sites (71%); severe gastrointestinal (GI) dysfunction (54%) and acute renal failure (43%). Crude 7-day and 30-day mortality rates were 20.6% and 39.7% respectively. Logistic regression multivariate analysis identified the following to be independent predictors for mortality: age > or =65 years [odds ratio (OR) 7.2, P = 0.013]; severe GI dysfunction (OR 10.6, P = 0.01); acute renal failure (OR 7.6, P = 0.022); recent/concurrent bacteraemia (OR 5.2, P = 0.042); endotracheal intubation (OR 7.7, P = 0.014); while major surgery was associated with a better prognosis (OR 0.05, P = 0.002). Appropriate antifungal treatment was also found to be associated with survival (Fisher's exact test, P < 0.001). The epidemiology of Candida bloodstream isolates within our health board had changed over the years. Incidence and mortality of candidaemia were relatively high in our hospital. Dysfunction of major organ systems and recent bacteraemia were found to predict mortality.
    • The 'carry-over' effects of patient self-testing: positive effects on usual care management by an anticoagulation management service.

      Ryan, Fiona; O'Shea, Susan; Byrne, Stephen; Pharmaceutical Care Research Group, School of Pharmacy, University College Cork, Cork, Ireland. (Elsevier, 2010-11)
      Patient self-testing (PST) of the international normalised ratio (INR) has a positive effect on anticoagulation control. This study investigated whether the benefits of PST (other than increased frequency of testing, e.g. patient education, empowerment, compliance etc.) could be 'carried-over' into usual care management after a period of home-testing has ceased.
    • Case 1. Unusual complications of a Hickman catheter.

      Horgan, Anne M; Kenny, Clodagh; Duffy, Austin; O'Reilly, Seamus; Cork University Hospital, Wilton, Cork, Ireland. (2012-02-03)
    • A case of deep burns, while diving The Lusitania.

      Curran, John N; McGuigan, Kevin G; O'Broin, Eoin; Department of Plastic, Reconstructive and Aesthetic Surgery, Cork University Hospital, Wilton, Cork, Ireland. curranjn@eircom.net (Elsevier, 2010-07)
      We present the first documented case of severe burns, sustained by a diver as a result of auto-ignition of air-activated heat packs at high partial pressure of oxygen and high ambient pressure. Our patient was diving the shipwreck of The Lusitania off the south coast of Ireland. This is a significant wreck, lying 90 metres down on the seabed. Torpedoed by a German U-boat in 1915, its loss prompted American involvement in WW1. Several unlikely events combined in this case to bring about serious and life threatening injuries. Herein we discuss the case and explore some of the physical and chemical processes that lead to these injuries.
    • Case of the month: an unusual cause of neck pain.

      Casey, M C; Lim, C; Hickey, M C; Department of Radiology, Cork University Hospital, Cork, Ireland. (2012-02-03)
    • A case report of spontaneous mutation (C33>U) in the iron-responsive element of L-ferritin causing hyperferritinemia-cataract syndrome.

      Cao, Wei; McMahon, Mary; Wang, Bo; O'Connor, Rosemary; Clarkson, Michael; Cell Biology Laboratory, Department of Biochemistry, University College Cork, Cork, Ireland. caowei_111@yahoo.com.cn (Elsevier, 2010-01-15)
      The hereditary hyperferritinemia cataract syndrome (HHCS) is an autosomal dominant disorder characterized by juvenile-onset cataracts and elevated serum ferritin levels. It is caused by mutation in the iron response element (IRE) within the 5'UTR of L-ferritin gene. The mutation results in a loss of post-transcriptional negative feedback exerted by the interaction between iron regulatory proteins 1, 2 (IRP1 and IRP2) and IRE, which leads to uncontrolled expression of L-ferritin. In this paper, we describe the molecular pathogenesis of non-hereditary hyperferritinemia cataract syndrome (non-H-HCS) in a patient with typical HHCS ocular lens morphology and high ferritin levels without obvious family history. Initial sequencing of the full-length L-ferritin cloned from genomic DNA demonstrated a mutation (C33>T) in the IRE of the affected patient but not in her unaffected family members. The mutation (C/T heterozygote) was also detected in cDNA derived from her blood mononuclear cells. Structure-prediction-modeling indicates that this mutation would significantly alter the secondary structure of the IRE, resulting in a loss of the interaction between IRP and IRE. By using IRP1/IRP2-human IgG1 Fc fusion proteins, we established a novel in vitro report system (modified ELISA) to verify impaired IRE/IRP binding. Both the C33>U and A40G mutations (the first identified mutation for HHCS) showed a dramatically decreased binding to IRP1/IRP2 protein, compared to the normal IRE RNA. Surprisingly, a decrease in L-ferritin mRNA levels was observed in the affected patient compared to controls suggesting a mechanism of transcriptional negative feedback by high intracellular L-ferritin protein levels not described heretofore. Taken together, spontaneous mutation in the IRE of L-ferritin may cause non-H-HCS by the same mechanism as HHCS. In addition, under abnormal circumstances, the protein level of L-ferritin may be principally controlled by post-transcriptional regulation rather than the transcriptional regulation. The successful establishment of an ELISA report system provides an alternative method to evaluate precisely the interaction between protein and RNA.
    • CD38 is associated with premenopausal and postmenopausal bone mineral density and postmenopausal bone loss.

      Drummond, Frances J; Mackrill, John J; O'sullivan, Kathleen; Daly, Mary; Shanahan, Fergus; Molloy, Michael G; Department of Rheumatology and Medicine, Clinical Sciences Building, Cork, University Hospital, National University of Ireland, Cork, Ireland., f.drummond@ncri.ie (2012-02-03)
      One goal of osteoporosis research is to identify the genes and environmental factors that contribute to low bone mineral density (BMD) and fracture. Linkage analyses have identified quantitative trait loci (QTLs), however, the genes contributing to low BMD are largely unknown. We examined the potential association of an intronic polymorphism in CD38 with BMD and postmenopausal bone loss. CD38 resides in 4p15, where a QTL for BMD has been described. CD38-/- mice display an osteoporotic phenotype at 3 months, with normalization of BMD by 5 months. The CD38 polymorphism was identified by polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) analysis in 457 postmenopausal and 173 premenopausal Caucasian women whose spine and hip BMD was measured by dual energy X-ray absorptiometry (DXA). Influence of the CD38 polymorphism on bone loss was analyzed in 273 postmenopausal women over a follow-up of 2.94 +/- 1.50 years. The CD38-PvuII polymorphism was significantly associated with premenopausal and postmenopausal (P = 0.001) lumbar spine BMD. Women homozygous for the G allele had >14% lower spinal BMD than women with GC/CC genotypes. An allele dose effect was observed at the spine in premenopausal (P = 0.002) and postmenopausal (P < 0.001) cohorts. The CD38-PvuII polymorphism was significantly associated with femoral neck BMD in pre- and postmenopausal women (P = 0.002 and P = 0.011, respectively). However, significance was lost following adjustment of hip BMD for covariates in the postmenopausal cohort (P = 0.081). The CD38-PvuII polymorphism was weakly associated with bone loss at the spine (P = 0.024), in postmenopausal women not taking hormone replacement therapy. We suggest that the CD38-PvuII polymorphism may influence the attainment and maintenance of peak BMD and postmenopausal bone loss.
    • Cell response to surgery.

      Ni Choileain, Niamh; Redmond, H Paul; Department of Surgery, Cork University Hospital, Wilton, Cork, Ireland., nncl@eircom.net (2012-02-03)
      OBJECTIVES: To describe the profound alterations in host immunity that are produced by major surgery as demonstrated by experimental and clinical studies, and to evaluate the benefits of therapeutic strategies aimed at attenuating perioperative immune dysfunction. DATA SOURCES: A review of the English-language literature was conducted, incorporating searches of the MEDLINE, EMBASE, and Cochrane collaboration databases to identify laboratory and clinical studies investigating the cellular response to surgery. STUDY SELECTION: Original articles and case reports describing immune dysfunction secondary to surgical trauma were included. DATA EXTRACTION: The results were compiled to show outcomes of different studies and were compared. DATA SYNTHESIS: Current evidence indicates that the early systemic inflammatory response syndrome observed after major surgery that is characterized by proinflammatory cytokine release, microcirculatory disturbance, and cell-mediated immune dysfunction is followed by a compensatory anti-inflammatory response syndrome, which predisposes the patient to opportunistic infection, multiple organ dysfunction syndrome, and death. Because there are currently no effective treatment options for multiple organ dysfunction syndrome, measures to prevent its onset should be initiated at an early stage. Accumulating experimental evidence suggests that targeted therapeutic strategies involving immunomodulatory agents such as interferon gamma, granulocyte colony-stimulating factor, the prostaglandin E(2) antagonist, indomethacin, and pentoxifylline may be used for the treatment of systemic inflammatory response syndrome to prevent the onset of multiple organ dysfunction syndrome. CONCLUSIONS: Surgical trauma produces profound immunological dysfunction. Therapeutic strategies directed at restoring immune homeostasis should aim to redress the physiological proinflammatory-anti-inflammatory cell imbalance associated with major surgery.
    • Cellular apoptosis and organ injury in sepsis: a review.

      Power, Colm; Fanning, Noel; Redmond, H Paul; Department of Academic Surgery, Cork University Hospital and University College, Cork, Ireland. (2012-02-03)
    • Cellular reprogramming by gram-positive bacterial components: a review.

      Buckley, Julliette M; Wang, Jiang Huai; Redmond, H Paul; Department of Academic Surgery, Cork University Hospital, National University of , Ireland/University College Cork, Wilton, Cork, Ireland. (2012-02-03)
      LPS tolerance has been the focus of extensive scientific and clinical research over the last several decades in an attempt to elucidate the sequence of changes that occur at a molecular level in tolerized cells. Tolerance to components of gram-positive bacterial cell walls such as bacterial lipoprotein and lipoteichoic acid is a much lesser studied, although equally important, phenomenon. This review will focus on cellular reprogramming by gram-positive bacterial components and examines the alterations in cell surface receptor expression, changes in intracellular signaling, gene expression and cytokine production, and the phenomenon of cross-tolerance.
    • A CF patient with progressive proteinuric renal disease: a CF-specific nodular glomerulosclerosis?

      O'Connell, O.; Magee, C. N.; Fitzgerald, B.; Burke, L.; Plant, W. D.; Plant, B. J. (2010)
    • "The challenge facing renal artery revascularization: what have we not proven and why we must"?

      Hynes, B G; Margey, R; Moran, D; Ruggiero, N J; Kiernan, T J; Jaff, M R; Section of Vascular Medicine, Division of Cardiology, Massachusetts General Hospital, Boston MA, USA. (2012-01-04)
      Endovascular renal artery stent therapy for atherosclerotic renal artery stenosis (RAS) is associated with excellent acute technical success, low complication rates and acceptable long-term patency. However, the clinical benefits to patients of renal artery stenting remain uncertain. To facilitate debate regarding the treatment of RAS, we need to understand the epidemiology, basic physiology and clinical consequences of renal artery stenosis. We must attempt to determine which patients are likely to benefit from renal artery stenting, assess the nuances of the percutaneous procedure and review the current literature pertaining to renal artery stenting.