Biomedical risk assessment as an aid for smoking cessation.

BACKGROUND: A possible strategy for increasing smoking cessation rates could be to provide smokers who have contact with healthcare systems with feedback on the biomedical or potential future effects of smoking, e.g. measurement of exhaled carbon monoxide (CO), lung function, or genetic susceptibility to lung cancer. OBJECTIVES: To determine the efficacy of biomedical risk assessment provided in addition to various levels of counselling, as a contributing aid to smoking cessation. SEARCH STRATEGY: We systematically searched the Cochrane Collaboration Tobacco Addiction Group Specialized Register, Cochrane Central Register of Controlled Trials 2008 Issue 4, MEDLINE (1966 to January 2009), and EMBASE (1980 to January 2009). We combined methodological terms with terms related to smoking cessation counselling and biomedical measurements. SELECTION CRITERIA: Inclusion criteria were: a randomized controlled trial design; subjects participating in smoking cessation interventions; interventions based on a biomedical test to increase motivation to quit; control groups receiving all other components of intervention; an outcome of smoking cessation rate at least six months after the start of the intervention. DATA COLLECTION AND ANALYSIS: Two assessors independently conducted data extraction on each paper, with disagreements resolved by consensus. Results were expressed as a relative risk (RR) for smoking cessation with 95% confidence intervals (CI). Where appropriate a pooled effect was estimated using a Mantel-Haenszel fixed effect method. MAIN RESULTS: We included eleven trials using a variety of biomedical tests. Two pairs of trials had sufficiently similar recruitment, setting and interventions to calculate a pooled effect; there was no evidence that CO measurement in primary care (RR 1.06, 95% CI 0.85 to 1.32) or spirometry in primary care (RR 1.18, 95% CI 0.77 to 1.81) increased cessation rates. We did not pool the other seven trials. One trial in primary care detected a significant benefit of lung age feedback after spirometry (RR 2.12; 95% CI 1.24 to 3.62). One trial that used ultrasonography of carotid and femoral arteries and photographs of plaques detected a benefit (RR 2.77; 95% CI 1.04 to 7.41) but enrolled a population of light smokers. Five trials failed to detect evidence of a significant effect. One of these tested CO feedback alone and CO + genetic susceptibility as two different intervention; none of the three possible comparisons detected significant effects. Three others used a combination of CO and spirometry feedback in different settings, and one tested for a genetic marker. AUTHORS' CONCLUSIONS: There is little evidence about the effects of most types of biomedical tests for risk assessment. Spirometry combined with an interpretation of the results in terms of 'lung age' had a significant effect in a single good quality trial. Mixed quality evidence does not support the hypothesis that other types of biomedical risk assessment increase smoking cessation in comparison to standard treatment. Only two pairs of studies were similar enough in term of recruitment, setting, and intervention to allow meta-analysis.

Estudi d’alteracions genètiques predictores de resposta al tractament amb cetuximab en càncer colorectal

Projecte de recerca elaborat a partir d’una estada al Cancer Center, Massachusetts General Hospital- Harvard School of Medicine, Boston, Estats Units entre gener i juny 2007. El desenvolupament de nous fàrmacs dirigits a dianes moleculars específiques ha suposat un gran avanç en el tractament del càncer. El millor coneixement dels mecanismes que determinen la sensibilitat a aquests tractaments biològics és crucial per poder oferir tractaments selectius, optimitzar l'índex terapèutic i controlar l'elevat cost d'aquests fàrmacs. Tal com ha demostrat el grup liderat pel Dr. Settleman i altres, la sensibilitat del tumor a nous fàrmacs dirigits a diana molecular ve determinada en part per alteracions genètiques de les cèl.lules tumorals. El paradigma és la resposta clínica a fàrmacs inhibidors tirosin-cinasa d’ EGFR dels pacients amb càncer de pulmó amb mutacions d'EGFR. Donada la importància de trobar marcadors predictors de sensibilitat a les noves teràpies biològiques, la detecció a gran escala d' alteraciones genètiques i las seva correlació amb la sensibilitat al tractament amb aquests fàrmacs en models preclínics és un primer pas essencial per a un posterior desenvolupament a nivell clínic. En aquest estudi vam establir una plataforma de cribatge d’alta densitat (high throughput screening) de línies cel.lulars que ens permet detectar alteracions genètiques predictores de resposta a fàrmacs dirigits a diana molecular específica. Presentem el desenvolupament d'aquesta plataforma i el resultat de dues aplicacions específiques(... )

A phase I dose-escalation study of the immunocytokine EMD 521873 (Selectikine) in patients with advanced solid tumours.

BACKGROUND: EMD 521873 (Selectikine), an immunocytokine comprising a DNA-targeting antibody, aimed at tumour necrosis, fused with a genetically modified interleukin-2 (IL-2) moiety, was investigated in this first-in-human phase I study. METHODS: Patients had metastatic or locally advanced solid tumours failing previous standard therapy. Selectikine was administered as a 1-hour intravenous infusion on 3 consecutive days, every 3weeks. A subgroup of patients also received 300mg/m(2) cyclophosphamide on day 1 of each cycle. Escalating doses of Selectikine were investigated with the primary objective of determining the maximum tolerated dose (MTD). RESULTS: Thirty-nine patients were treated with Selectikine alone at dose levels from 0.075 to 0.9mg/kg, and nine were treated at doses of 0.45 and 0.6mg/kg in combination with cyclophosphamide. A dose-dependent linear increase of peak serum concentrations and area under curve was found. The dose-limiting toxicity was grade 3 skin rash at the 0.9mg/kg dose-level; the MTD was 0.6mg/kg. Rash and flu-like symptoms were the most frequent side-effects. No severe cardiovascular side-effects (hypotension or vascular leak) were observed. At all dose-levels, transient increases in total lymphocyte, eosinophil and monocyte counts were recorded. No objective tumour responses, but long periods of disease stabilisation were observed. Transient and non-neutralising Selectikine antibodies were detected in 69% of patients. CONCLUSIONS: The MTD of Selectikine with or without cyclophosphamide administered under this schedule was 0.6mg/kg. The recommended phase II dose was 0.45-0.6mg/kg. Selectikine had a favourable safety profile and induced biological effects typical for IL-2.

Recent developments in the use of chemotherapy in brain tumours.

Several recent studies have further clarified the role of chemotherapy in newly diagnosed anaplastic glioma. For newly diagnosed glioblastoma, combined daily radiotherapy with daily temozolomide followed by six cycles of adjuvant temozolomide improves overall survival. This benefit is especially observed in patients with a methylated promotor of the MGMT gene which encodes an alkyltransferase; this observation however, needs confirmation. Although oligodendroglial tumours are sensitive to chemotherapy, classical adjuvant nitrosourea-based chemotherapy does not improve overall survival in newly diagnosed anaplastic oligodendroglioma, even in the subset of 1p/19q loss tumours. It may increase progression-free survival however, and further studies must show if combined modality treatment with daily chemotherapy during radiotherapy increases survival. Trials exploring the role of chemotherapy in low-grade glioma are ongoing. No standard chemotherapy is currently available for highly anaplastic glioma failing first-line temozolomide-based therapy.

Intellectual outcome in children and adolescents with acute lymphoblastic leukaemia treated with chemotherapy alone: age- and sex-related differences.

One of the most relevant concerns in long-term survivors of paediatric acute lymphoblastic leukaemia (ALL) is the development of neuropsychological sequelae. The majority of the published studies report on patients treated with chemotherapy and prophylactic central nervous system (CNS) irradiation, little is known about the outcome of patients treated with chemotherapy-only regimens. Using the standardised clinical and neuropsychological instruments of the SPOG Late Effects Study, the intellectual performance of 132 paediatric ALL patients treated with chemotherapy only was compared to that of 100 control patients surviving from diverse non-CNS solid tumours. As a group, ALL and solid tumour survivors showed normal and comparable intellectual performances (mean global IQ 104.6 in both groups). The percentage of patients in the borderline range (global IQ between 70 and 85) was comparable and not higher as expected (10% cases and 13% controls, expected 16%). Only 2 (2%) of the former ALL and 1 (1%) of the solid tumour patients were in the range of mental retardation (global IQ<70). Former known risk factors described in children treated with prophylactic CNS irradiation, like a younger age at diagnosis of ALL and female gender, remained valid in chemotherapy-only treated patients. The abandonment of prophylactic CNS irradiation and its replacement by a more intensive systemic and intrathecal chemotherapy led to a reduction, but not the disappearance of late neuropsychological sequelae.

Review of therapeutic drug monitoring of anticancer drugs part one - Cytotoxics.

Most anticancer drugs are characterised by a steep dose-response relationship and narrow therapeutic window. Inter-individual pharmacokinetic (PK) variability is often substantial. The most relevant PK parameter for cytotoxic drugs is the area under the plasma concentration versus time curve (AUC). Thus it is somewhat surprising that therapeutic drug monitoring (TDM) is still uncommon for the majority of agents. Goals of the review were to assess the rationale for more widely used TDM of cytotoxics in oncology. There are several reasons why TDM has never been fully implemented into daily oncology practice. These include difficulties in establishing appropriate concentration target ranges, common use of combination chemotherapies for many tumour types, analytical challenges with prodrugs, intracellular compounds, the paucity of published data from pharmacological trials and 'Day1=Day21' administration schedules. There are some specific situations for which these limitations are overcome, including high dose methotrexate, 5-fluorouracil infusion, mitotane and some high dose chemotherapy regimens. TDM in paediatric oncology represents an important challenge. Established TDM approaches includes the widely used anticancer agents carboplatin, busulfan and methotrexate, with 13-cis-retinoic acid also recently of interest. Considerable effort should be made to better define concentration-effect relationships and to utilise tools such as population PK/PD models and comparative randomised trials of classic dosing versus pharmacokinetically guided adaptive dosing. There is an important heterogeneity among clinical practices and a strong need to promote TDM guidelines among the oncological community.

NovoTTF-100A versus physician's choice chemotherapy in recurrent glioblastoma: A randomised phase III trial of a novel treatment modality.

PURPOSE: NovoTTF-100A is a portable device delivering low-intensity, intermediate frequency electric fields via non-invasive, transducer arrays. Tumour Treatment Fields (TTF), a completely new therapeutic modality in cancer treatment, physically interfere with cell division. METHODS: Phase III trial of chemotherapy-free treatment of NovoTTF (20-24h/day) versus active chemotherapy in the treatment of patients with recurrent glioblastoma. Primary end-point was improvement of overall survival. RESULTS: Patients (median age 54years (range 23-80), Karnofsky performance status 80% (range 50-100) were randomised to TTF alone (n=120) or active chemotherapy control (n=117). Number of prior treatments was two (range 1-6). Median survival was 6.6 versus 6.0months (hazard ratio 0.86 [95% CI 0.66-1.12]; p=0.27), 1-year survival rate was 20% and 20%, progression-free survival rate at 6months was 21.4% and 15.1% (p=0.13), respectively in TTF and active control patients. Responses were more common in the TTF arm (14% versus 9.6%, p=0.19). The TTF-related adverse events were mild (14%) to moderate (2%) skin rash beneath the transducer arrays. Severe adverse events occurred in 6% and 16% (p=0.022) of patients treated with TTF and chemotherapy, respectively. Quality of life analyses favoured TTF therapy in most domains. CONCLUSIONS: This is the first controlled trial evaluating an entirely novel cancer treatment modality delivering electric fields rather than chemotherapy. No improvement in overall survival was demonstrated, however efficacy and activity with this chemotherapy-free treatment device appears comparable to chemotherapy regimens that are commonly used for recurrent glioblastoma. Toxicity and quality of life clearly favoured TTF.

Individual versus standard quality of life assessment in a phase II clinical trial in mesothelioma patients: feasibility and responsiveness to clinical changes.

BACKGROUND: In patients with malignant pleural mesothelioma undergoing a multimodality therapy, treatment toxicity may outweigh the benefit of progression-free survival. The subjective experience across different treatment phases is an important clinical outcome. This study compares a standard with an individual quality of life (QoL) measure used in a multi-center phase II trial. PATIENTS AND METHODS: Sixty-one patients with stage I-III technically operable pleural mesothelioma were treated with preoperative chemotherapy, followed by pleuropneumonectomy and subsequent radiotherapy. QoL was assessed at baseline, at day 1 of cycle 3, and 1, 3 and 6 months post-surgery by using the Rotterdam Symptom Checklist (RSCL) and the Schedule for the Evaluation of Quality of Life-Direct Weighting (SEIQoL-DW), a measure that is based on five individually nominated and weighted QoL-domains. RESULTS: Completion rates were 98% (RSCL) and 92% (SEIQoL) at baseline and 98%/89% at cycle 3, respectively. Of the operated patients (N=45) RSCL and SEIQoL were available from 86%/72%, 93%/74%, and 94%/76% at months 1, 3, and 6 post-surgery. Average assessment time for the SEIQoL was 24min compared to 8min needed for the RSCL. Median changes from baseline indicate that both RSCL QoL overall score and SEIQoL index remained stable during chemotherapy with a clinically significant deterioration (change>or=8 points) 1 month after surgery (median change of -66 and -14 for RSCL and SEIQoL, respectively). RSCL QoL overall scores improved thereafter, but remained beneath baseline level until 6 months after surgery. SEIQoL scores improved to baseline-level at month 3 after surgery, but worsened again at month 6. RSCL QoL overall score and SEIQoL index were moderately correlated at baseline (r=.30; p<or=.05) and at 6-month follow-up (r=.42; p<or=.05) but not at the other time points. CONCLUSION: The SEIQoL assessment seems to be feasible within a phase II clinical trial, but may require more effort from staff. More distinctive QoL changes in accordance with clinical changes were measured with the RSCL. Our findings suggest that the two measures are not interchangeable: the RSCL is to favor when mainly information related to the course of disease- and treatment is of interest.

The tumour suppressor LATS2 interacts with both Signalosome and E3 ubiquitin ligases : implications in control of cell cycle progression

SUMMARY LATS2 is a member of the Lats tumour suppressor gene family. The human LATS2 gene is located at chromosome 13q11-12, which has been shown to be a hot spot (67%) for LOH in nonsmall cell lung cancer. Both lats mosaic flies and LATS1 deficient mice spontaneously develop tumours, an observation that is explained by the function of LATS1 in suppressing tumourigenesis by negatively regulating cell proliferation by modulating Cdc2/Cyclin A activity. LATS1 also plays a critical role in maintenance of ploidy through its action on the spindle assembly checkpoint. Initial insights into the function of LATS2 reveals that the protein is involved in the G2/M transition of the cell cycle, whereby it controls the phosphorylation status of Cdc25C. The aim of the present study was to identify LATS2 interacting partners that would provide a more thorough understanding of the molecular pathways in which the protein is involved. The yeast two-hybrid system identified a number of candidate genes that interact with LATS2. Most of the interactions were confirmed biochemically by GST-pull down assays that enabled us to demonstrate that LATS2 is an integral component of the Signalosome complex. The Signalosome is thought to be required for the establishment of functional Cullin-based E3 ubiquitin ligases, the substrate-recognition elements of the ubiquitin-mediated protein proteolytic pathway. The findings that LATS2 also interacts with all of the components of the E3 enzymes allows us to postulate that LATS2 is probably involved in the regulation of this Signalosome-E3 super-complex. In addition, the discovery that LATS2 associates with multiple protein kinases localised at the cellular membrane and in various signalling cascades supports the idea that LATS2 functions as an integrator of signals which allows it to monitor the activity of these pathways and translate these signals through its action on the Signalosome. Furthermore, the observation that a kinase-dead LATS2 mutant arrests at the G2/M phase of the cell cycle, demonstrates that the protein, through the action of its kinase domain, is crucial for progression through the cell cycle, an action in accordance to its proposed role as a regulator of E3 ubiquitin ligases. The findings presented herein provide evidence that LATS2 associates with the Signalosome-E3 ubiquitin ligases super-complex which governs protein stability. Any alteration of the protein would have a strong impact on pathways that modulate cell proliferation, as shown by its implication in tumourigenesis. RESUME LATS2 est un membre de la famille de gènes suppresseurs de tumeurs LATS. Le gène humain LATS2 est situé sur le chromosome 13q11-12, une région qui s'est avérée être un point sensible (67%) dans la perte d'hétérozigosité (LOH) notamment pour le cancer du poumon. Le fait que des tumeurs se développent spontanément chez les souris qui sont déficientes pour le gène LATS1 ainsi que dans des cellules mutantes pour LATS chez la Drosophile, est expliqué Par la fonction de LATS1, qui est de supprimer l'apparition de tumeurs en réprimant la prolifération cellulaire à travers sa capacité à réguler l'activité de Cdc2/Cyciine A. LATS1 joue également un rôle important au niveau du maintient de la ploïdie de la cellule, au travers de son action sur les points de contrôle de l'assemblage du fuseau mitotique. Les premières études du gène LATS2 indiquent que la protéine est, par son contrôle des réactions de phosphorylation de la Cdc25C, impliquée dans la transition 021M. Le but de cette étude était d'identifier les protéines qui interagissent avec LATS2, en vue d'obtenir une compréhension plus approfondie des mécanismes moléculaires dans lesquels LATS2 se trouve engagée. Le système de double-hybride chez la levure a permis l'identification d'un grand nombre de gènes qui interagissent avec LATS2. La plupart des interactions ont été confirmées par GST «pull clown», une technique in vitro qui a permis de démontrer que LATS2 est un composant intégral du Signalosome. Ce complexe est supposé réguler l'activité des E3 ubiquitine-rigases, les éléments responsables du recrutement des substrats qui doivent être recyclés par la voie de dégradation ubiquitine-dépendante. Les résultats obtenus indiquent également que LATS2 interagit avec tous les composants des enzymes E3, ce qui nous permet de soumettre l'idée selon laquelle la protéine LATS2 est en fait impliquée dans la régulation du complexe Signalosorne-E3. De plus, la découverte que LATS2 se trouve associée à plusieurs protéines kinases localisées au niveau de la membrane cellulaire, ainsi que dans diverses voies de transduction, confirment l'idée que LATS2 fonctionne en tant que molécule qui intègre les signaux en provenance de ces différentes voies cellulaires. De ce fait, il lui serait possible de coordonner la destruction des protéines au moyen du complexe Signalosome, permettant ainsi de réprimer l'activité des voies de signalisation. En outre, l'introduction d'une mutation dans le domaine kinase de LATS2 résulte en l'arrêt du cycle cellulaire en G2/M, ce qui montre que la protéine, au travers de son domaine kinase, est cruciale pour le bon fonctionnement du cycle cellulaire, ceci en accord avec son rôle proposé comme régulateur des E3 ubiquitine-ligases. Les résultats présentés dans ce manuscrit démontrent que la protéine LATS2 se trouve associée au complexe Signalosome-E3 qui régule la dégradation des protéines. La moindre modification de la protéine engendrerait des répercussions importantes au niveau des voies de transduction qui contrôlent fa prolifération ceilulaire, ce qui atteste du rôle déterminant que joue LAT32 dans la tumorigénèse.

Occupational exposure of truck drivers to dust and polynuclear aromatic hydrocarbons: a pilot study in Geneva, Switzerland.

The exposure to dust and polynuclear aromatic hydrocarbons (PAH) of 15 truck drivers from Geneva, Switzerland, was measured. The drivers were divided between "long-distance" drivers and "local" drivers and between smokers and nonsmokers and were compared with a control group of 6 office workers who were also divided into smokers and nonsmokers. Dust was measured on 1 workday both by a direct-reading instrument and by sampling. The local drivers showed higher exposure to dust (0.3 mg/m3) and PAH than the long-distance drivers (0.1 mg/m3), who showed no difference with the control group. This observation may be due to the fact that the local drivers spend more time in more polluted areas, such as streets with heavy traffic and construction sites, than do the long-distance drivers. Smoking does not influence exposure to dust and PAH of professional truck drivers, as measured in this study, probably because the ventilation rate of the truck cabins is relatively high even during cold days (11-15 r/h). The distribution of dust concentrations was shown in some cases to be quite different from the expected log-normal distribution. The contribution of diesel exhaust to these exposures could not be estimated since no specific tracer was used. However, the relatively low level of dust exposure dose not support the hypothesis that present day levels of diesel exhaust particulates play a significant role in the excess occurrence of lung cancer observed in professional truck drivers.

I. Identification and characterisation of epigenetically altered tumor supressor genes by proteomic and genomic approches / II. Studies of genes regualted by MeCP2 union to its promoter regions by proteomic and genmomic approches

DNA methylation has an important impact on normal cell physiology, thus any defects in this mechanism may be related to the development of various diseases In this project we are interested in identifying epigeneticaliy modified genes, in general controlled by processes related to the DNA methylation, by means of a new strategy combining protomic and genomic analyses. First, the two Dimensional-Difference Gel Electrophoresis (2-DIGE) protein analyses of extracts obtained from HCT-116 wt and double knockout for DNMT1 and DNMT3b (DKO) cells revealed 34 proteins overexpressed in the condition of DNMTs depletion. From five genes with higher transcript lavels in DKO cells, comparing with HCT-116 wt. oniy AKR1B1, UCHLl and VIM are melhylated in HCT-116. As expected. the DNA methvlation 1s lost in DKO cells. The rneth,vl ation of VIM and UCHLl promoters in some cancer samples has already been repaired, thus further studies has been focused on AKRlBI. AKR1B1 expression due lo DNA methyiaton of promoter region seems to occur specilfically in the colon cancer cell Iines. which was confirmed in the DNA rnethylation status and expression analyses. performed on 32 different cancer cell lines (including colon, breast, lymphoma, leukemia, neuroblastoma, glioma and lung cancer cell Iines) as well as normal colon and normal lymphocytes samples. AKRIBI expression after treatments with DNA demethvlating agent (AZA) was rescued in 5 coloncancer cell lines (including genetic regulation of the candidate gene. The methylation status of the rest of the genes identified in proteomic analysis was checked by methylation specific PCR (MSP) experiment and all appeared to be unmethylated. The similar research has been done also bv means of Mecp2-null mouse model For 14 selected candidate genes the analyses of expression leveis, methylation Status and MeCP2 interaction with promoters are currently being performed.

University Research Proposal Submission Topics 2010

Dietetics Rectal Tumours and Pressure Relief Physio and Pilates with Gynae Cancer PatientsPhysio Nordic Walking and Breast CancerNeuro RehabRelaxation and Lung Cancer Physio for a Haematology Exercise Scheme - Cancer Related Fatigue Strategies Physio Classes and Prostate CancerRehab - Malignant Spinal Cord Compression and Rehab needs Seating.

Consultation launched on Community Development Strategy - your views matter

Issued jointly by the Health and Social Care Board and Public Health AgencyThe Health and Social Care Board and the Public Health Agency have today launched, for public consultation, a new Community Development Strategy.The consultation period will run for 12 weeks from Friday 10 June until Friday 2 September 2011.The Board and Agency want to see strong, resilient communities where everyone has good health and wellbeing, places where people look out for each other and have community pride in where they live.Residents from deprived areas in Northern Ireland experience;lower life expectancy;higher rates of emergency admission to hospital;higher rates of lung cancer;higher rates of suicide; andhigher rates of smoking and alcohol related deaths.The kinds of health and social care issues which can be improved by community development approaches include depression; isolation; falls amongst elderly people; child protection; teenage pregnancy; childhood asthma; postnatal depression; drug and alcohol abuse; and ultimately also long term conditions such as obesity, diabetes and cancer.The Board and Agency seek a number of benefits from implementing this strategy such as; a reduction in health and wellbeing inequalities, which also means addressing the social factors that affect health; strengthening partnership working with service users, the community and voluntary sectors and other organisations; strengthening families and communities; supporting volunteering and making best use of our resources.John Compton, Chief Executive of the Health and Social Care Board said: "Community development is an important way to improving health and wellbeing - driving a message that 'prevention is better than cure' between different groups and communities, and helping to ensure the most effective use of the health and social care budget."Now more than ever we need to work in partnership with families and communities to achieve better health and wellbeing for those living in Northern Ireland.No one organisation can meet this challenge on its own and strong partnerships are needed. "Chief Executive of the Public Health Agency, Eddie Rooney added: "Every health and social care organisation should incorporate a community development approach into their programmes, and this strategy assists them to do so."The Board and Agency have jointly held pre-consultation workshops over the past few months across Northern Ireland on their Community Development Strategy and have engaged widely with the community and voluntary sectors. We are now keen to receive feedback from individuals, families and the wider community as your views are very important to us - they will help shape the future of community development across the province," he said.The draft Community Development Strategy, as well as information on how you can respond, can be found in the attachments below.

Functional assessment of chest wall integrity after methylmethacrylate reconstruction.

BACKGROUND: All patients with extensive resection of the anterolateral chest wall and the sternum followed by reconstruction with methylmethacrylate substitutes were assessed prospectively 6 months after the operation to delineate chest wall integrity with pulmonary function and cine-magnetic resonance imaging. METHODS: Twenty-six patients underwent chest wall reconstruction by use of methylmethacrylate between 1994 and 1998 due to primary tumors in 35%, metastases in 27%, T3 lung cancer in 19%, and debridement for radionecrosis and osteomyelitis in 19% of patients. Three to eight ribs were resected and additional sternum resection was performed in 39% of patients. RESULTS: There was no 30-day mortality. All patients were extubated after the operation without need for reintubation. Prosthesis dislocation occurred in 1 patient and infection in 2 patients during follow-up. Nineteen patients (73%) suffered no restrictions of daily activities. Clinical examination revealed normal shoulder girdle function in 77% of patients. There was no significant difference between preoperative and postoperative FEV1 (forced expiratory volume in 1 second) measurements in patients with lobectomy or wedge resections. Cinemagnetic resonance imaging revealed concordant chest wall movements during respiration in 92% of patients without paradoxical movements or implant dislocations being observed. CONCLUSIONS: Large defects of the anterolateral chest wall and sternum can be reconstructed efficiently with methylmethacrylate substitutes with minimal morbidity and excellent cosmetic and functional outcome.

Passive smoking there's nothing passive about it

This poster highlights how passive smoking increases your risk of lung cancer, heart disease, asthma and stroke.