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Premature Death (premature + death)
Selected AbstractsSmoking and Risk of Premature Death among Middle-aged Japanese: Ten-year Follow-up of the Japan Public Health Center-based Prospective Study on Cancer and Cardiovascular Diseases (JPHC Study) Cohort ICANCER SCIENCE, Issue 1 2002Megumi Hara To update the evidence on the association between smoking and mortality, we analyzed data from a population-based prospective study in Japan. In total, 19 950 men and 21 534 women aged 40,59 who reported their smoking history and had no serious disease at baseline survey were followed. During 1990,1999, 1014 men and 500 women died. Smokers were associated with an unhealthy life-style. Relative risks (RRs) for selected cause of death due to smoking were slightly attenuated by adjusting for possible confounding factors. Age- and area-adjusted RRs of male current smokers compared with never smokers were 1.66 (95% confidence intervals (CI): 1.40, 1.95) for all causes, 1.69 (1.31, 2.18) for all cancers, 1.67 (1.20, 2.34) for all circulatory system disease, and 1.63 (1.24, 2.15) for other causes, while those of females were 2.03 (1.52, 2.73), 2.06 (1.35, 3.15), 2.99 (1.75, 5.11), 1.31 (0.69, 2.51), respectively. After adjusting for multivariate variables, the corresponding RRs of male smokers were 1.55 (1.29, 1.86), 1.61 (1.20, 2.15), 1.41 (0.97, 2.03), and 1.61 (1.17, 2.19), against 1.89 (1.36, 2.62), 1.83 (1.14, 2.95), 2.72 (1.45, 5.07), and 1.39 (0.71, 2.73) for females. Twenty-two percent of death from all causes, 25% of all cancer, and 17% of all circulatory system disease deaths, could be attributed to cigarette smoking in males, and 5%, 4%, and 11% in females, respectively. Cumulative dose as indicated by pack-years was clearly associated with cancer death. These findings provided information as to the quantitative risk for premature death due to smoking among middle-aged Japanese men and women, and showed that the elevated risk was not explained by the unhealthy lifestyle of smokers. [source] Prediction of mortality at age 40 in Danish males at high and low risk for alcoholismACTA PSYCHIATRICA SCANDINAVICA, Issue 6 2004J. Knop Objective:, This prospective high-risk study examined the influence of father's alcoholism and other archival-generated measures on premature death. Method:, Sons of alcoholic fathers (n = 223) and sons of non-alcoholic fathers (n = 106) have been studied from birth to age 40. Archival predictors of premature death included father's alcoholism, childhood developmental data, and diagnostic information obtained from the Psychiatric Register and alcoholism clinics. Results:, By age 40, 21 of the 329 subjects had died (6.4%), a rate that is more than two times greater than expected. Sons of alcoholic fathers were not more likely to die by age 40. Premature death was associated with physical immaturity at 1-year of age and psychiatric/alcoholism treatment. No significant interactions were found between risk and archival measures. Conclusion:, Genetic vulnerability did not independently predict death at age 40. Death was associated with developmental immaturities and treatment for a psychiatric and/or substance abuse problem. [source] SCN5A Mutation Associated with Cardiac Conduction Defect and Atrial ArrhythmiasJOURNAL OF CARDIOVASCULAR ELECTROPHYSIOLOGY, Issue 5 2006PÄIVI J. LAITINEN-FORSBLOM Ph.D. Introduction: We aimed at identifying the molecular defect underlying the clinical phenotype of a Finnish family with a cardiac conduction defect and atrial arrhythmias. Methods and Results: A large Finnish family was clinically evaluated (ECG, 24-hour ambulatory ECG, echocardiography). We performed linkage analysis with markers flanking the SCN5A gene and subsequently sequenced the SCN5A gene. Five family members had atrial arrhythmias and intracardiac conduction defects, and due to bradycardia needed a pacemaker when adolescents. No heart failure or sudden cardiac death was observed. Left ventricle dilatation was seen in one individual and three individuals had a slightly enlarged right ventricle. Premature death due to stroke occurred in one subject during the study, and two other members had suffered from stroke at young age. Linkage analysis favored the role of the SCN5A gene in disease pathogenesis, and direct sequencing disclosed D1275N mutation. This alteration was present not only in all six affected individuals, but also in two young individuals lacking clinical symptoms. Conclusions: Cardiac conduction defect and atrial arrhythmias in a large Finnish family appear to result from the SCN5A D1275N mutation. Although no sudden cardiac death was recorded in the family, at least three affected members had encountered brain infarction at the age of 30 or younger. [source] Premature death among teenage mothersBJOG : AN INTERNATIONAL JOURNAL OF OBSTETRICS & GYNAECOLOGY, Issue 8 2004Petra Otterblad Olausson Objective Some data suggest an association between teenage childbearing and premature death. Whether this possible increase in risk is associated with social circumstances before or after childbirth is not known. We studied premature death in relation to age at first birth, social background and social situation after first birth. Design Population-based cohort study. Setting Women born in Sweden registered in the 1985 Swedish Population Census. Population Swedish women born 1950,1964 who had their first infant before the age of 30 years (N= 460,434). Methods Information on the women's social background and social situation after first birth was obtained from Population Censuses. The women were followed up with regard to cause of death from December 1, 1990 to December 31, 1995. Mortality rate ratios and 95% confidence intervals (CI) were calculated. Main outcome measures Mortality rates by cause of death. Results Independent of socio-economic background, teenage mothers faced an increased risk of premature death later in life compared with older mothers (rate ratio 1.6, 95% CI 1.4,1.9). The increased risk was most evident for deaths from cervical cancer, lung cancer, ischaemic heart disease, suicide, inflicted violence and alcohol-related diseases. Some, but not all, of these increases in risk were associated with the poorer social position of teenagers mothers. Conclusions Teenage mothers, independent of socio-economic background, face an increased risk of premature death. Strategies to reduce teenage childbearing are likely to contribute to improved maternal and infant health. [source] Increasing Self-Management Skills in Heart Failure Patients: A Pilot StudyCONGESTIVE HEART FAILURE, Issue 6 2005Kristin J. Flynn PhD Nonadherence to medical treatment among heart failure patients is high and results in frequent exacerbations and premature death. This treatment-only pilot study examined whether a year-long group-based self-management intervention is feasible and improves self-management skills in patients with mild-to-moderate heart failure (ejection fraction ,40% and New York Heart Association functional class I, II, or III). A total of 31 of 100 recruited patients (31%) agreed to participate. Twenty-six (84%) completed the year-long self-management program. Compared with baseline, the intervention was associated with an increase in overall self-efficacy in practicing self-management skills (p<0.001) and in four of five specific self-management skills. Patients and their group leaders also reported an increase in actual use of self-management skills (p<0.001) and in several psychosocial outcomes. The success of this pilot study suggests the need for a randomized clinical trial to test the efficacy of group-based self-management training on medical outcomes. [source] Food and Poverty: Insights from the ,North'DEVELOPMENT POLICY REVIEW, Issue 5-6 2003Elizabeth Dowler The role that food and nutrition play in the material definitions of poverty are contrasted with the social construction of malnutrition and poverty, drawing largely on British experience. The consequences for poor health and premature death are briefly examined; in particular, the connection is made to the world-wide growth in obesity, and in cardio-vascular disease, cancers and diabetes. The lived experience of those defined as poor in the North, and the implications of contemporary policy initiatives and responses by state, private and voluntary sectors, are explored. The challenges of the dominant policy framework remain consumer and individual choice, rather than public health and citizenship, which militates against the realisation of true food security. [source] Which comes first: atypical antipsychotic treatment or cardiometabolic risk?ACTA PSYCHIATRICA SCANDINAVICA, Issue 3 2009S. M. Stahl Objective:, To provide an overview for practicing clinicians on the pharmacological basis of cardiometabolic risk induced by antipsychotic drugs in patients with serious mental illness, to propose hypotheses to explain these risks and to give tips for managing cardiometabolic risk during antipsychotic treatment. Method:, A MEDLINE search using terms for atypical antipsychotics (including individual drug names), metabolic, cardiovascular, weight gain and insulin resistance, cross-referenced with schizophrenia was performed on articles published between 1990 and May 2008. Results:, Strong evidence exists for significant cardiometabolic risk differences among several antipsychotic agents. Histamine H1 and serotonin 5HT2C antagonism are associated with risk of weight gain, but receptor targets for dyslipidemia and insulin resistance have not yet been identified. Convincing data indicate that hypertriglyceridemia and insulin resistance may occur in the absence of weight gain with certain antipsychotics. Conclusion:, Although lifestyle and genetics may contribute independent risks of cardiometabolic dysfunction in schizophrenia and other serious mental illness, antipsychotic treatment also represents an important contributor to risk of cardiometabolic dysfunction, particularly for certain drugs and for vulnerable patients. Mental health professionals must learn to recognize the clinical signposts indicating antipsychotic-related cardiometabolic problems to forestall progression to type II diabetes, cardiovascular events and premature death. [source] Prediction of mortality at age 40 in Danish males at high and low risk for alcoholismACTA PSYCHIATRICA SCANDINAVICA, Issue 6 2004J. Knop Objective:, This prospective high-risk study examined the influence of father's alcoholism and other archival-generated measures on premature death. Method:, Sons of alcoholic fathers (n = 223) and sons of non-alcoholic fathers (n = 106) have been studied from birth to age 40. Archival predictors of premature death included father's alcoholism, childhood developmental data, and diagnostic information obtained from the Psychiatric Register and alcoholism clinics. Results:, By age 40, 21 of the 329 subjects had died (6.4%), a rate that is more than two times greater than expected. Sons of alcoholic fathers were not more likely to die by age 40. Premature death was associated with physical immaturity at 1-year of age and psychiatric/alcoholism treatment. No significant interactions were found between risk and archival measures. Conclusion:, Genetic vulnerability did not independently predict death at age 40. Death was associated with developmental immaturities and treatment for a psychiatric and/or substance abuse problem. [source] Global use of alcohol, drugs and tobaccoDRUG AND ALCOHOL REVIEW, Issue 6 2006PETER ANDERSON Abstract Humans have always used drugs, probably as part of their evolutionary and nutritional heritage. However, this previous biological adaptation is unlikely to be so in the modern world, in which 2 billion adults (48% of the adult population) are current users of alcohol, 1.1 billion adults (29% of the adult population) are current smokers of cigarettes and 185 million adults (4.5% of the adult population) are current users of illicit drugs. The use of drugs is determined largely by market forces, with increases in affordability and availability increasing use. People with socio-economic deprivation, however measured, are at increased risk of harmful drug use, as are those with a disadvantaged family environment, and those who live in a community with higher levels of substance use. Substance use is on the increase in low-income countries which, in the coming decades, will bear a disproportionate burden of substance-related disability and premature death. [source] Drugs and violent death: comparative toxicology of homicide and non-substance toxicity suicide victimsADDICTION, Issue 6 2009Shane Darke ABSTRACT Aims To determine the comparative toxicology of death by homicide and suicide by means other than substance toxicity. Design Cross-sectional (autopsy reports). Setting Sydney, Australia. Cases A total of 1723 cases of violent death were identified, comprising 478 homicide (HOM) cases and 1245 non-substance toxicity suicide (SUI) cases. Findings Substances were detected in 65.5% of cases, and multiple substances in 25.8%, with no group differences. Illicit drugs were detected in 23.9% of cases, and multiple illicit in 5.3%. HOM cases were significantly more likely to have an illicit drug [odds ratio (OR) 2.09] and multiple illicits (OR 2.94), detected, HOM cases being more likely to have cannabis (OR 2.39), opioids (OR 1.53) and psychostimulants (OR 1.59) present. HOM cases were, however, significantly less likely to have benzodiazepines (OR 0.53), antidepressants (OR 0.22) and antipsychotics (OR 0.23) present. Alcohol was present in 39.6% of cases (median blood alcohol concentration = 0.12), with no group difference in prevalence. Conclusions The role drugs play in premature death extends far beyond overdose and disease, with illicit drugs associated strongly with homicide. [source] Why should addiction medicine be an attractive field for young physicians?ADDICTION, Issue 2 2009Michael Soyka ABSTRACT Aims The clinical practice and science of addiction are increasingly active fields, which are attracting professionals from diverse disciplines such as psychology and neurobiology. Our scientific knowledge of the pathophysiology of addiction is rapidly growing, along with the variety of effective treatments available to clinicians. Yet, we believe that the medical specialties of addiction medicine/psychiatry are not attracting the interest and enthusiasm of young physicians. What can be done? Methods We offer the opinions of two experience addiction psychiatrists. Results In the US, there has been a decline in the number of psychiatrists seeking training or board certification in addiction psychiatry; about one-third of graduates with such training are not practicing in an addiction psychiatry setting. There is widespread neglect of addiction medicine/psychiatry among the medical profession, academia and national health authorities. This neglect is unfortunate, given the enormous societal costs of addiction (3,5% of the gross domestic product in some developed countries), the substantial unmet need for addiction treatment, and the highly favourable benefit to cost yield (at least 7:1) from treatment. Conclusions We believe that addiction medicine/psychiatry can be made more attractive for young physicians. Helpful steps include widening acceptance as a medical specialty or subspecialty, reducing the social stigma against people with substance use disorders, expanding insurance coverage and increasing the low rates of reimbursement for physicians. These steps would be easier to take with broader societal (and political) recognition of substance use disorders as a major cause of premature death, morbidity and economic burden. [source] Eating disorders in females with type 1 diabetes: an update of a meta-analysisEUROPEAN EATING DISORDERS REVIEW, Issue 4 2002Søren Nielsen Abstract Objective: Firstly to provide a quantitative summary of existing studies on the occurrence of eating disorders (ED) in females with type 1 diabetes (IDDM), with the focus on retinopathy and insulin misuse for the different eating disorders. Secondly to disseminate knowledge about useful statistical tools. Research Design and Methods: Data were extracted from the relevant case,control and follow-up studies. Odds ratios (OR) and risk differences (RD) were the main effect sizes analysed. Analyses were based on ,exact' methods as many studies are sparse. Data and findings are presented in sufficient detail for re-analysis. Results: An hypothesis of an increase in Anorexia Nervosa (AN) in IDDM is not supported by existing evidence. Bulimia Nervosa is increased (OR,=,2.9 (95%CI: 1.03 to 8.4); pOR,=,0.04) in IDDM. Both ED-NOS and subthreshold ED is increased (OR ,2; pOR,<,0.001) in females with IDDM. Co-existing ED in IDDM increases the overall common OR for retinopathy to 4.8 (95%CI: 3.0 to 7.8); pOR,<,0.00001, and the overall mean RD is 33% (95%CI: 25% to 42%); pRD,<,0.001. Insulin misuse (IM) is increased when ED co-exists with IDDM: OR 12.6 (95%CI: 7.8 to 21.1); pOR,<,0.00001, and mean RD is 40% (95%CI: 29% to 50%); pRD,<,0.001. Conclusions: ED-NOS and subthreshold ED seem to be the quantitatively most important EDs in type 1 diabetic females. Mismanagement of diabetes in the form of IM is frequent in eating disordered IDDM probands. Early occurrence of retinopathy and other complications is an increased risk in concurrent cases, as is premature death. The implications of Binge Eating Disorder (BED) and overweight needs to be elucidated for both type 1 and type 2 diabetes. Copyright © 2002 John Wiley & Sons, Ltd and Eating Disorders Association. [source] Fabry disease: overall effects of agalsidase alfa treatmentEUROPEAN JOURNAL OF CLINICAL INVESTIGATION, Issue 12 2004M. Beck Abstract Background, Fabry disease is a rare X-linked disorder caused by deficient activity of the lysosomal enzyme ,-galactosidase A. Progressive accumulation of the substrate globotriaosylceramide in cells throughout the body leads to major organ failure and premature death. The Fabry Outcome Survey (FOS) is a European outcomes database which was established to collect data on the natural history of this little-known disease and to monitor the long-term efficacy and safety of enzyme replacement therapy (ERT) with agalsidase alfa. This paper presents the first analysis of the FOS database on the effects of ERT on renal function, heart size, pain and quality of life. Design, The effects of 1 and 2 years of ERT with agalsidase alfa on renal function (assessed by estimated glomerular filtration rate), heart size (assessed by echocardiography), pain (assessed by the Brief Pain Inventory) and quality of life (assessed by the European Quality of Life Questionnaire EQ-5D) were analyzed in a cohort of 545 patients, 314 of whom were receiving treatment (188 for at least 12 months and 92 for at least 24 months; mean duration of treatment, 17 months; maximum duration, 56 months). Results, Treatment with agalsidase alfa stabilized renal function in patients with a mild or moderate deterioration in renal function at baseline, reduced left ventricular size in patients who had an enlarged heart at baseline, and improved pain scores and quality of life. These improvements were similar in hemizygous men and heterozygous women with Fabry disease. Conclusions, Enzyme replacement therapy with agalsidase alfa leads to significant clinical benefits in patients with Fabry disease, and treatment is likely to alter the natural history of this disorder. [source] Altered longevity-assurance activity of p53:p44 in the mouse causes memory loss, neurodegeneration and premature deathAGING CELL, Issue 2 2010Mariana Pehar Summary The longevity-assurance activity of the tumor suppressor p53 depends on the levels of ,40p53 (p44), a short and naturally occurring isoform of the p53 gene. As such, increased dosage of p44 in the mouse leads to accelerated aging and short lifespan. Here we show that mice homozygous for a transgene encoding p44 (p44+/+) display cognitive decline and synaptic impairment early in life. The synaptic deficits are attributed to hyperactivation of insulin-like growth factor 1 receptor (IGF-1R) signaling and altered metabolism of the microtubule-binding protein tau. In fact, they were rescued by either Igf1r or Mapt haploinsufficiency. When expressing a human or a ,humanized' form of the amyloid precursor protein (APP), p44+/+ animals developed a selective degeneration of memory-forming and -retrieving areas of the brain, and died prematurely. Mechanistically, the neurodegeneration was caused by both paraptosis- and autophagy-like cell deaths. These results indicate that altered longevity-assurance activity of p53:p44 causes memory loss and neurodegeneration by affecting IGF-1R signaling. Importantly, Igf1r haploinsufficiency was also able to correct the synaptic deficits of APP695/swe mice, a model of Alzheimer's disease. [source] Homocysteine, the MTHFR 677 C,T polymorphism and family history of premature cardiovascular diseaseJOURNAL OF HUMAN NUTRITION & DIETETICS, Issue 3 2009A. Carey Background:, Cardiovascular disease (CVD) is the main cause of premature death in the UK and accounts for 36% of all premature male deaths and 27% of female deaths every year (British Heart Foundation, 2006). Although many risk factors for CVD are known, family history has been identified as being of particular importance in premature CVD (Lloyd-Jones et al., 2004). Recently, it was suggested that an elevated homocysteine (tHcy) may be associated with premature CVD (Homocystiene Studies Collaboration, 2002). The main genetic determinant of tHcy is the common 677 C,T polymorphism, in the enzyme methylenetetrahydrofolate reductase (MTHFR), which is prevalent in approximately 10% of the UK population. Relatively few studies have examined the association between tHcy and premature CVD and hardly any have considered the role of this polymorphism. The aim of this study therefore was to examine the relationships between the MTHFR 677 C,T polymorphism, tHcy and a family history of CVD in patients with established premature CVD. Methods:, An analysis was conducted on medical, lifestyle and family history data collected from patients and age-sex matched controls, recruited through the GENOVIT study in 2003. This case,control study involved n = 404 premature CVD patients and a similar number of age-sex matched controls, all of whom were screened for the TT genotype. A subset of patients (n = 196) and controls (n = 167) provided a blood sample, from which the tHcy concentration was established. Independent sample t -tests were used to determine differences between patients and controls and differences among genotype groups were examined using a one-way analysis of variance, followed by a Tukey's post hoc test. Results:, Plasma tHcy was significantly elevated in patients with a family history of CVD (compared to those without) (P = 0.013). A nonsignificant trend towards higher tHcy (compared to those without) was observed in patients with the TT genotype (P = 0.419). Furthermore, specifically in those with the TT genotype, those with a family history of CVD (compared to those without) showed significantly higher tHcy concentrations (P < 0.005). Those with the TT genotype who smoked had significantly higher tHcy (P < 0.05) than the CC and CT genotypes. Discussion:, The findings presented provide evidence to support an association between the MTHFR 677C,T polymorphism, elevated homocysteine and family history of premature CVD. Given that dietary levels of riboflavin have been shown to lower homocysteine specifically in individuals with the TT genotype (McNulty et al., 2006), these results have implications for the dietary management of premature CVD in those individuals with a genetic predisposition for elevated tHcy. In conclusion, further research in larger cohort numbers, regarding the correlation between family history, tHcy and the MTHFR polymorphism, would be beneficial for establishing their cause and effect relationship. References British Heart Foundation (2006) All Deaths and Deaths Under 75 by Cause and Sex, 2005, England, Wales, Scotland, N Ireland and United Kingdom. Available at http://www.bhf.org.uk/research_health_professionals/resources/heart_statistics.aspx. Homocystine Studies Collaboration (2002) Homocysteine and the risk of ishaemic heart disease and stroke. JAMA288, 2015,2022. Llyod-Jones, D.M., Nam, B.H., D'Agostino, R.B., Levy, D., Murabito, J.M., Wang, T.J., Wilson, P.W. & O'Donnell, C.J. (2004) Parental cardiovascular disease as a risk factor for cardiovascular disease in middle-aged adults, a prospective study of parents and offspring. JAMA291, 2204,2211. McNulty, H., Dowey le, R.C., Strain, J.J., Dunne, A., Ward, M., Molloy, A.M., McAnena. L.B., Hughes, J.P., Hannon-Fletcher, M. & Scott, J.M. Riboflavin lowers homocysteine in individuals homozygous for the MTHFR 677C->T polymorphism. Circulation113, 74,80. [source] Metabolic syndrome, its preeminent clusters, incident coronary heart disease and all-cause mortality , results of prospective analysis for the Atherosclerosis Risk in Communities studyJOURNAL OF INTERNAL MEDICINE, Issue 1 2007Y. Hong Abstract. Objective., To investigate the prospective association between Metabolic Syndrome (MetS) and coronary heart disease (CHD) and all-cause mortality. Subjects and Design., A bi-racial cohort of 14 699 middle-aged Americans from the Atherosclerosis Risk in Communities study were followed for the development of new CHD and death over a period of 9 years. MetS, using the original ATP-III criteria, was defined as having at least three of the following components: elevated blood pressure (BP), elevated plasma glucose, elevated blood triglyceride (TG), increased waist circumference, and low HDL cholesterol (HDL-c). Incident CHD cases included hospitalized myocardial infarction (MI), fatal CHD, revascularization procedures, and silent MI as detected by EKG. Results., The prevalence of the MetS at baseline was 29%, 30%, 40% and 26% among CHD-free white women, white men, black women, and black men, respectively. There were 1018 incident CHD cases and 1039 deaths. The relative risk (RR) and 95% confidence interval (CI) of incident CHD associated with MetS was 2.46 (1.99, 3.03) for women and 1.86 (1.59, 2.18) for men. Clear dose,response relationship between the number of MetS components and incidence of CHD was found (P for linear trend <0.001). The following three clusters of MetS components posed the highest risk for CHD: (i) the elevated BP and glucose and low HDL-c group [RR = 5.68 (3.44, 9.37)]; (ii) the elevated BP and glucose and TG group [RR = 5.08 (2.96, 8.70)]; and (iii) the elevated BP and TG and low HDL-c group [RR = 3.98 (2.75, 5.77)]. When all five components co-existed, the risk was the highest [RR = 6.24 (4.65, 8.36)]. Similar results with attenuated RR were found for all-cause mortality. Conclusions., Individuals, especially women, with the MetS have significantly higher risk of developing CHD. The riskiest combination is high-BP and glucose clustered with low HDL-c or high TG. These data highlight the importance of targeting MetS in the prevention of CHD and premature death. [source] A ,Catch Up' Plan for radiotherapy in New South Wales to 2012JOURNAL OF MEDICAL IMAGING AND RADIATION ONCOLOGY, Issue 4 2009Graeme Morgan Summary In New South Wales (NSW) from 1996 to 2006, only 34,37% of newly diagnosed cancer patients were treated with radiotherapy instead of the 50% proposed by NSW Health in Radiotherapy Plans released in 1991, 1995 and 2003. As a consequence, over 50 000 cancer patients were not treated and has resulted in the estimated premature death of over 8000 patients and over 40 000 years of life lost. In 2008, there were 42 linear accelerators in NSW rather than the 62 recommended. Based on cancer incidence projections, NSW will require 69 linear accelerators in 2012 , a shortfall of 27 linear accelerators. Already 15 linear accelerators have been approved. NSW Health has funding for seven extra linear accelerators, and eight extra linear accelerators are to be funded by the private sector. To make up the shortfall, a ,Catch Up' Plan is proposed for an additional 12 linear accelerators by the end of fiscal year 2012. This is estimated to cost $200 million over 4 years for one-off establishment costs for buildings and equipment plus $50 million per year for recurrent operating costs such as staff salaries. The ,Catch Up' Plan will create five new departments of radiation oncology in country hospitals and three new departments in metropolitan hospitals. These will be in addition to those already approved by NSW Health and will markedly improve access for treatment and result in an improvement in cancer survival. This significant increase in departments and equipment can only be achieved by the creation of an NSW Radiotherapy Taskforce similar to that proposed in the Baume report of 2002, ,A vision for radiotherapy'. Even if the ,Catch Up' Plan bridges the gap in service provision, forward planning beyond 2012 should commence immediately as 76 linear accelerators will be required for NSW in 2015 and 81 linear accelerators in 2017. [source] Regional and Developmental Expression of the Npc1 mRNA in the Mouse BrainJOURNAL OF NEUROCHEMISTRY, Issue 3 2000A. Prasad Abstract: Niemann-Pick type C (NP-C) disease is a fatal, autosomal recessive disorder of cholesterol metabolism that results in progressive central nervous system deterioration and premature death. Recently, a gene mutated in NP-C disease (NPC1) was identified in both human patients and in the npcnih mouse model. Although the function of the NPC1 gene is at present unknown, determining the pattern of its expression in the brain may facilitate identification of the mechanisms underlying the neuropathology of this disease and in identifying relevant targets for any potential therapeutic intervention. We have used in situ hybridization techniques to characterize the pattern of Npc1 mRNA expression in both the wild-type and the npcnih mutant mouse brain. In adult animals of both genotypes, the Npc1 mRNA was detected in the majority of neurons in nearly all regions, but at significantly higher levels in the cerebellum and in specific pontine nuclei. Analysis of Npc1 mRNA levels during development in the wild-type mouse indicated that this transcript was expressed in neurons as early as embryonic day 15 and that a significant region-specific pattern of expression was established by postnatal day 7. Our data suggest that whereas the NPC1 gene is widely expressed in neurons of the brain, the higher levels of expression in the cerebellum and pontine structures established by early postnatal ages may make these regions more susceptible to neuronal dysfunction in NP-C disease. [source] Kisspeptin: A Novel Regulator of Reproductive FunctionJOURNAL OF NEUROENDOCRINOLOGY, Issue 8 2008W. S. Dhillo Young Neuroendocrinologists Prize Reviews Michael Harbuz Young Investigator Prize Lecture The UK and international neuroendocrine community was deeply shocked and saddened the unbelievably premature death of Michael Harbuz in Bristol in 2006. Mick was a superb friend and colleague, and played a huge part in the development and activities of the British Neuroendocrine Group/British Society for Neuroendocrinology (BSN), serving as both Membership Secretary and Treasurer between 1999 and 2004. Mick was a leader in the field of neuroendocrine,immune interactions, and brought a great deal of charisma, humour and ability to meetings and conferences. He was also a passionate and committed supporter of the progress of young researchers and of their participation in neuroendocrine events. He recognised that today's postgraduate students and postdoctoral research fellows are tomorrow's neuroendocrine researchers, be it in academia, the health services or industry. To recognise Mick's great commitment to and enthusiasm for postgraduate education both in the University of Bristol and in the BSN, we decided to honour and remember him by instituting the ,Michael Harbuz Young Investigator Prize Lecture' to be delivered annually. Dr Waljit Dhillo from Imperial College London was the inaugural recipient of this award, and presented his lecture at the Annual Meeting of the BSN in Nottingham in September 2007, upon which this review is based. Recent evidence demonstrates that the neuropeptide kisspeptin and its receptor, GPR54, have a fundamental role in initiating the onset of puberty and are important in regulating reproductive function. This review discusses the evidence available from animals and humans demonstrating that kisspeptin potently stimulates the release of gonadotrophins by stimulating the release of gonadotrophin-releasing hormone and that a lack of kisspeptin or GPR54 results in reproductive failure. [source] Ocular phenotype in a mouse gene knockout model for infantile neuronal ceroid lipofuscinosisJOURNAL OF NEUROSCIENCE RESEARCH, Issue 5 2006Bo Lei Abstract Mutations in the human protein palmitoyl thioesterase-1 (PPT-1) gene result in an autosomal recessive neurodegenerative disorder designated neuronal ceroid lipofuscinosis (NCL), type CLN1, or infantile NCL. Among the symptoms of the CLN1 disease are accumulation of autofluorescent lysosomal storage bodies in neurons and other cell types, seizures, motor and cognitive decline, blindness, and premature death. Development of an effective therapy for this disorder will be greatly assisted by the availability of suitable animal models. A mouse PPT-1 gene knockout model has recently been generated. Studies were performed to determine whether the mouse model exhibits ocular features of the human CLN1 disorder. A progressive accumulation of autofluorescent storage material in all layers of the retina was observed in the PPT-1 knockout mice. Accompanying the storage body accumulation was a modest loss of cells with nuclei in the outer and inner nuclear layers. As indicated by electroretinogram (ERG) responses, retinal function was only mildly impaired at 4 months of age but was severely impaired by 8 months, despite only modest changes in retinal morphology. The pupillary light reflex (PLR), on the other hand, was exaggerated in the knockout mice. The apparent anomaly between the ERG and the PLR findings suggests that disease-related PLR changes may be due to changes in extraocular signal processing. The pronounced ocular phenotype in the PPT-1 knockout mice makes these animals a good model for testing therapeutic interventions for treatment of the human CLN1 disorder. © 2006 Wiley-Liss, Inc. [source] Physician attitudes towards ventilatory support for spinal muscular atrophy type 1 in AustralasiaJOURNAL OF PAEDIATRICS AND CHILD HEALTH, Issue 12 2007Nimeshan Geevasinga Background: Without ventilatory support, premature death from respiratory insufficiency is virtually universal in infants with spinal muscular atrophy type 1 (SMA1). With mechanical ventilation, however, long-term survival has been reported from numerous international centres. We aimed to characterize physician attitudes to the various forms of ventilatory support for children with SMA1. Methods: We surveyed neurologists, respiratory physicians, clinical geneticists and intensivists from all major paediatric hospitals in Australia and New Zealand regarding their views on ventilatory management of SMA1. Results: Ninety-two of the 157 (59%) physicians surveyed replied. Respondents included 16 clinical geneticists, 19 intensive care physicians, 28 neurologists and 29 respiratory physicians. Almost half (47%) opposed invasive ventilation of children with SMA1 and respiratory failure precipitated by intercurrent illness. The majority (76%) opposed invasive ventilatory support for chronic respiratory failure in SMA1. In contrast, non-invasive ventilation was felt by 85% to be appropriate for acute respiratory deteriorations, with 49% supporting long-term non-invasive ventilatory support. Most physicians felt that decisions regarding ventilation should be made jointly by parents and doctors, and that hospital Clinical Ethics Committees should be involved in the event of discordant opinion regarding further management. A majority felt that a defined hospital policy would be valuable in guiding management of SMA1. Conclusions: Respiratory support in SMA1 is an important issue with significant ethical, financial and resource management implications. Most physicians in Australian and New Zealand oppose invasive ventilatory support for chronic respiratory failure in SMA1. Non-invasive ventilation is an accepted intervention for acute respiratory decompensation and may have a role in the long-term management of SMA1. Clinical Ethics Committees and institutional policies have a place in guiding physicians and parents in the management of children with SMA1. [source] Periodontitis and premature death: a 16-year longitudinal study in a Swedish urban populationJOURNAL OF PERIODONTAL RESEARCH, Issue 4 2007B. Söder Background and Objective:, Growing experimental evidence implicates chronic inflammation/infection due to periodontal diseases as a risk factor for death. The objective was to evaluate the role of periodontitis in premature death in a prospective study. Methods:, The causes of death in 3273 randomly-selected subjects, aged 30,40 years, from 1985 to 2001 were registered. At baseline, 1676 individuals underwent a clinical oral examination (Group A) and 1597 did not (Group B). Mortality and causes of death from 1985 to 2001 were recorded according to ICD-9-10. Results:, In Groups A (clinically examined group) and B, a total of 110 subjects had died: 40 subjects in Group A, and 70 in Group B. In Group A significant differences were present at baseline between survivors and persons who later died, with respect to dental plaque, calculus, gingival inflammation and number of missing molars in subjects with periodontitis (p < 0.001). The multiple logistic regression analysis results of the relationship between being dead (dependent variable) and several independent variables identified periodontitis with any missing molars as a principal independent predictor of death. Conclusions:, Young individuals with periodontitis and missing molars seem to be at increased risk for premature death by life-threatening diseases, such as neoplasms, and diseases of the circulatory and digestive systems. [source] GABRA2 and Alcohol Use Disorders: No Evidence of an Association in an Italian Case,Control StudyALCOHOLISM, Issue 4 2010Nicoletta Onori Background:, Alcoholism is a major health and social issue, a highly frequent disease and a cause of premature death. It is also the most expensive addictive disorder being related to high morbidity and mortality, violence, accidents, and social and legal problems. It is a quantitative disorder, where the combined incidence of environmental and multiple genetic factors varies from 1 subject to another. Recent association studies have identified several genes as candidates for alcoholism, including GABAA receptor genes, due to their role in mediating several behavioral effects of alcohol, such as motor incoordination, anxiolysis, sedation, and withdrawal. The proposed association between the 3, half of the gene encoding the alpha-2 subunit of GABA receptor (3,-GABRA2) and alcohol use disorders (AUDs) has received several independent confirmations. Methods:, In this study, 10 single nucleotide polymorphisms (SNPs) of the 3,-GABRA2 gene, previously reported to be implicated in alcohol dependence, were used to evaluate the linkage between selected SNPs and AUDs in an Italian sample and to compare findings with those of previous studies. Results:, No evidence of an association was found at the allele, genotype, haplotype, or diplotype levels between the 3,-GABRA2 polymorphisms investigated and alcoholism in 149 Italian alcoholics (98 alcohol dependents and 51 alcohol abusers) and 278 controls. Conclusions:, Despite previous reports, we did not find an association between AUDs and 3,-GABRA2 polymorphisms. This is probably due to the minimal comorbidity of our Italian sample suggesting that this gene is implicated in polysubstance dependence rather than in alcoholism alone. [source] Nucleation and facilitation in salt pans in Mediterranean salt marshesJOURNAL OF VEGETATION SCIENCE, Issue 6 2001A.E. Rubio-Casal Tutin et al. (1992) Abstract. Arthrocnemum macrostachyum is a perennial species acting as a primary colonizer of salt pans in Mediterranean high salt marshes. Salicornia ramosissima, an annual, occurs in salt pans under Arthrocnemum canopies and in open areas. The aim of this study was to analyse, in wild populations and a transplant experiment, how S. ramosissima population dynamics and growth are affected by A. macrostachyum. The environmental conditions within the patches of Arthrocnemum were less stressful than in the open areas, with lower radiation levels and salinity concentrations. In the inner areas of A. macrostachyum patches, density-dependent mortality processes of S. ramosissima seedlings led to low densities of adult individuals with greater morphological development and reproductive success than in open areas. However, at the edges of Arthrocnemum patches facilitation of seedling survival favoured high densities. Environmental stress hindered development, decreased reproduction and premature death. These results are in agreement with the general theory of factors controlling vegetation distribution that biotic interactions dominate in low stress environments, while abiotic interactions dominate under harsher environmental conditions. A. macrostachyum plays an essential role in the succession in these salt pans, facilitating seed production and stimulating nucleation processes in S. ramosissima. [source] What is the real gain after liver transplantation?LIVER TRANSPLANTATION, Issue S2 2009James Neuberger Key Points 1. For most liver allograft recipients, both the quality and length of life are greatly improved after transplantation. However, neither the quality of life nor the length of life in the survivors returns to that seen in age-matched and sex-matched normal subjects. 2. The gain in survival after transplantation can be estimated by a comparison of the actual outcome after transplantation and the predicted survival in the absence of transplantation. 3. The reduction in graft and patient survival, in comparison with a normal age-matched and sex-matched population, is determined by several factors: short-term survival is affected by the patient's condition pre-transplant and the quality of the graft, and for longer term survival, recurrent disease accounts for most of the differences seen between different indications. Some of the causes of premature death (such as infection, de novo malignancy, and cardiovascular and cerebrovascular disease) that are increased in the liver allograft recipient may be reduced by improved management with more aggressive surveillance and treatment. 4. The aims of selection and allocation vary in different health care systems: transparency, objectivity, equity of access, justice, mortality awaiting transplantation, utility, and transplant benefit are all important but often competing demands. Understanding the associated increase in survival will allow for a rational approach to this complex area. Liver Transpl 15:S1,S5, 2009. © 2009 AASLD. [source] Combined orthotopic heart and liver transplantation: The need for exception status listing1,LIVER TRANSPLANTATION, Issue 12 2004Paige M. Porrett Through May 2004, 33 combined orthotopic heart-liver transplants (OHT/OLT) have been performed nationwide. No published data exist to date regarding outcomes of patients awaiting such transplants, although progression of two organ disease processes may contribute to premature death for waiting patients. Retrospective data were collected on patients listed for combined OHT/OLT from both an individual tertiary care transplant center and the national UNOS registry to delineate listing criteria and evaluate patient outcomes in both the pre- and post-MELD eras. All patients who survived to transplantation or died on the waiting list were included in the analysis. Results show that 29.6% of patients registered nationally and 42% of patients listed institutionally survived to transplantation. Survival to transplantation was associated with less severe liver disease, though patients with MELD scores ranging from 19 to 26 had significantly higher wait list mortality than expected when compared to single-organ liver transplants. Following combined orthotopic heart-liver transplantation, 80% and 70% of patients survive 1 and 3 years, respectively. In conclusion, combined OHT/OLT is a successful therapy, but current organ allocation policies may not ensure expeditious transplantation in critically ill patients with dual vital organ failure. Providing exception status listing to these patients would ensure more expeditious transplantation and potentially contribute to improved survival. (Liver Transpl 2004;10:1539,1544.) [source] Left ventricular hypertrophy in chronic renal failure patientsNEPHROLOGY, Issue 2002Henry KRUM SUMMARY: Left ventricular hypertrophy is an important risk factor for cardiovascular disease, which is a major component of premature death among renal failure patients. Early treatment of progressive renal insufficiency has the opportunity to attempt prevention of, or reduction in, the development of LVH. Therapies specifically targeted at regression of LVH (e.g. antihypertensive regimens and epoetin-,) may, therefore, impact favourably on future cardiovascular events. Importantly, these approaches appear complementary and should be used in unison to maximize cardiovascular risk reduction in renal failure patients. [source] Frontotemporal dementia with motor neuron disease (amyotrophic lateral sclerosis with dementia)NEUROPATHOLOGY, Issue 1 2000Imaharu Nakano Frontotemporal dementia (FTD) with motor neuron disease means amyotrophic lateral sclerosis (ALS) with dementia. In the cerebrum of this condition, the medial cortex of the rostral temporal lobe is constantly and most remarkably involved. Another constant and quite characteristic lesion is neuronal loss localized to the CA1-subiculum transitional area at the level of the pes hippocampi. The rostral portion of the parahippocampal gyrus, and the amygdaloid nucleus are also involved. Ubiquitinated intracytoplasmic inclusions are seen in the dentate granule cells and parahippocampal gyrus neurons. Some cases of ALS without dementia show the identical temporal lobe degeneration as well as the cortical ubiquitinated inclusions, thus raising the possibility of overlooked dementia or premature death of the patients. Similarly, recently proposed motor neuron disease-inclusion dementia may be a forme fruste of ALS with dementia. [source] Intentional weight loss and mortality among initially healthy men and womenNUTRITION REVIEWS, Issue 7 2008Mette K Simonsen Most prospective observational studies suggest that weight loss increases the risk of premature death among obese individuals. This is surprising because clinical studies show that weight loss generally leads to overall improvements in cardiovascular risk factors. It is sometimes argued that the increased mortality observed with weight loss must depend on confounding or poor study designs. This review was conducted to summarize results from studies on intentional weight loss and mortality among healthy individuals, while carefully considering the designs and problems in these studies. Evaluation criteria with a rating scale were developed. Of the studies evaluated, two found decreased mortality with intentional weight loss, three found increased mortality, and four found no significant associations between intentional weight loss and total mortality. Thus, it is still not possible for health authorities to make secure recommendations on intentional weight loss. More studies designed to specifically address this issue are warranted. [source] Energy Regulation and Aging: Recent Findings and Their ImplicationsNUTRITION REVIEWS, Issue 4 2000Susan B. Roberts Ph.D. Old age is a time of vulnerability to unintentional weight loss, a factor that is associated with increased morbidity and premature death. Many possible causes of weight loss in old age have been suggested. The so-called anorexia of aging may play a particular role, by either reducing food intake directly or reducing food intake in response to such adverse factors as age-associated reductions in taste and smell, poor dentition, use of multiple prescription medicines, and depression. Recent studies also raise the question of whether a reduction in dietary variety may be important. These findings emphasize the need for regular monitoring of body weight to detect unintentional weight loss in older individuals and suggest testable ways to minimize the impact of the anorexia of aging on body weight through improved dietary management. [source] | |||||||||||||||||||||||||||||||||||||