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Multisystem inflammatory syndrome in children (MIS-C) is a complication of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection; in the United States, reporting of MIS-C after coronavirus disease 2019 (COVID-19) vaccination is required for vaccine safety monitoring. Pfizer-BioNTech COVID-19 vaccine was authorized for children aged 5-11 years on 29 October 2021. Covering a period when approximately 7 million children received vaccine, surveillance for MIS-C ≤ 90 days postvaccination using passive systems identified 58 children with MIS-C and laboratory evidence of past/recent SARS-CoV-2 infection, and 4 without evidence. During a period with extensive SARS-CoV-2 circulation, MIS-C illness in children after COVID-19 vaccination who lacked evidence of SARS-CoV-2 infection was rare (<1 per million vaccinated children)., Competing Interests: Potential conflicts of interest. S. K.'s institution has received funding from National Institutes of Health (NIH) to conduct clinical trials of Moderna and Janssen COVID-19 vaccines, and funding from Pfizer to conduct clinical trials of Pfizer-BioNTech COVID-19 vaccines. M. A. S. reports funding from NIH, CDC, Pfizer, and Merck; and royalties from UpToDate. K. E. reports grant funding from NIH and CDC; consultant to Bionet, GSK, and IBM; and membership of Data Safety and Monitoring Board for Sanofi, X-4 Pharma, Seqirus, Moderna, Pfizer, Merck, and Roche. C. B. C. reports grants from NIH and Merck; royalties from UpToDate; consulting fees from GlaxoSmithKline, Horizon Pharma, Premier Healthcare, Pfizer, Moderna, Cowen Investments, and Vindico; payment for medicolegal testimony from multiple firms (none related to this investigation); a US patent for staphylococcal antibody (number 10 981 979); participation on a data safety monitoring board or advisory board for Astellas; and is President of the Pediatric Infectious Diseases Society. E. P. S. reports grants from the NIH and Pfizer; consulting fees from Sanofi Pasteur; and serves on the Data Safety Monitoring Board for vaccine trials sponsored by the NIH's Division of Microbiology and Infectious Diseases. All other authors report no potential conflicts. All authors have submitted the ICMJE Form for Disclosure of Potential Conflicts of Interest. Conflicts that the editors consider relevant to the content of the manuscript have been disclosed., (Published by Oxford University Press on behalf of Infectious Diseases Society of America 2023.)

Despite reductions over the past 2 decades, childhood mortality remains high in low- and middle-income countries in sub-Saharan Africa and South Asia. In these settings, children often die at home, without contact with the health system, and are neither accounted for, nor attributed with a cause of death. In addition, when cause of death determinations occur, they often use nonspecific methods. Consequently, findings from models currently utilized to build national and global estimates of causes of death are associated with substantial uncertainty. Higher-quality data would enable stakeholders to effectively target interventions for the leading causes of childhood mortality, a critical component to achieving the Sustainable Development Goals by eliminating preventable perinatal and childhood deaths. The Child Health and Mortality Prevention Surveillance (CHAMPS) Network tracks the causes of under-5 mortality and stillbirths at sites in sub-Saharan Africa and South Asia through comprehensive mortality surveillance, utilizing minimally invasive tissue sampling (MITS), postmortem laboratory and pathology testing, verbal autopsy, and clinical and demographic data. CHAMPS sites have established facility- and community-based mortality notification systems, which aim to report potentially eligible deaths, defined as under-5 deaths and stillbirths within a defined catchment area, within 24-36 hours so that MITS can be conducted quickly after death. Where MITS has been conducted, a final cause of death is determined by an expert review panel. Data on cause of death will be provided to local, national, and global stakeholders to inform strategies to reduce perinatal and childhood mortality in sub-Saharan Africa and South Asia., (© The Author(s) 2019. Published by Oxford University Press for the Infectious Diseases Society of America.)

Background: Knowledge of preventable disease and differences in disease burden can inform public health action to improve health and health equity. We quantified the future lung cancer burden preventable by behavioural modifications across Australia., Methods: We pooled seven Australian cohort studies (n = 367 058) and linked them to national registries to identify lung cancers and deaths. We estimated population attributable fractions and their 95% confidence intervals (CIs) for modifiable risk factors, using risk estimates from the cohort data and risk factor exposure distribution from contemporary national health surveys., Results: During the first 10-year follow-up, there were 2025 incident lung cancers and 20 349 deaths. Stopping current smoking could prevent 53.7% (95% CI, 50.0-57.2%) of lung cancers over 40 years and 18.3% (11.0-25.1%) in 10 years. The smoking-attributable burden is highest in males, those who smoke <20 cigarettes per day, are <75 years of age, unmarried, of lower educational attainment, live in remote areas or are healthy weight. Increasing physical activity and fruit consumption, if causal, could prevent 15.6% (6.9-23.4%) and 7.5% (1.3-13.3%) of the lung cancer burden, respectively. Jointly, the three behaviour modifications could prevent up to 63.0% (58.0-67.5%) of lung cancers in 40 years, and 31.2% (20.9-40.1%) or 43 300 cancers in 10 years. The preventable burden is highest among those with multiple risk factors., Conclusions: Smoking remains responsible for the highest burden of lung cancer in Australia. The uneven burden distribution distinguishes subgroups that could benefit the most from activities to control the world's deadliest cancer.

Background: Previous estimates of the colorectal cancer (CRC) burden attributed to behaviors have not considered joint effects, competing risk, or population subgroup differences., Methods: We pooled data from seven prospective Australian cohort studies (n = 367 058) and linked them to national registries to identify CRCs and deaths. We estimated the strength of the associations between behaviors and CRC risk using a parametric piecewise constant hazards model, adjusting for age, sex, study, and other behaviors. Exposure prevalence was estimated from contemporary National Health Surveys. We calculated population attributable fractions for CRC preventable by changes to current behaviors, accounting for competing risk of death and risk factor interdependence. Statistical tests were two-sided., Results: During the first 10 years of follow-up, there were 3471 incident CRCs. Overweight or obesity explained 11.1%, ever smoking explained 10.7% (current smoking 3.9%), and drinking more than two compared with two or fewer alcoholic drinks per day explained 5.8% of the CRC burden. Jointly, these factors were responsible for 24.9% (95% confidence interval [CI] = 19.7% to 29.9%) of the burden, higher for men (36.7%) than women (13.2%, P difference < .001). The burden attributed to these factors was also higher for those born in Australia (28.7%) than elsewhere (16.8%, P difference = .047). We observed modification of the smoking-attributable burden by alcohol consumption and educational attainment, and modification of the obesity-attributable burden by age group and birthplace., Conclusions: We produced up-to-date estimates of the future CRC burden attributed to modifiable behaviors. We revealed novel differences between men and women, and other high-CRC burden subgroups that could potentially benefit most from programs that support behavioral change and early detection.

The ocular microenvironment has adapted several negative regulators of inflammation to maintain immune privilege and health of the visual axis. Several constitutively produced negative regulators within the eye TGF-β2, α-melanocyte stimulating hormone (α-MSH), Fas ligand (FasL), and PD-L1 standout because of their capacity to influence multiple pathways of inflammation, and that they are part of promoting immune tolerance. These regulators demonstrate the capacity of immune privilege to prevent the activation of inflammation, and to suppress activation of effector immune cells even under conditions of ocular inflammation induced by endotoxin and autoimmune disease. In addition, these negative regulators promote and expand immune cells that mediate regulatory and tolerogenic immunity. This in turn makes the immune cells themselves negative regulators of inflammation. This provides for a greater understanding of immune privilege in that it includes both molecular and cellular negative regulators of inflammation. This would mean that potentially new approaches to the treatment of autoimmune disease can be developed through the use of molecules and cells as negative regulators of inflammation., (©2018 Society for Leukocyte Biology.)

Study Objectives: To determine the relationship between obstructive sleep apnea (OSA) and chronic kidney disease (CKD). Previous population studies of the association are sparse, conflicting and confined largely to studies of administrative data., Methods: Cross-sectional analysis in unselected participants of the Men Androgens Inflammation Lifestyle Environment and Stress (MAILES) study, aged >40 years. Renal data were available for 812 men without a prior OSA diagnosis who underwent full in-home polysomnography (Embletta X100) in 2010-2011. CKD was defined as an estimated glomerular filtration rate (eGFR) <60 mL/min/1.73m2 or eGFR≥60 and albuminuria (albumin-creatinine ratio ≥3.0 mg/mmol)., Results: CKD (10.5%, n = 85 [Stage 1-3, 9.7%; Stage 4-5, 0.7%]) of predominantly mild severity showed significant associations with OSA (apnea-hypoapnea index [AHI] ≥ 10): odds ratio (OR) = 1.9, 95% confidence interval (CI): 1.02-3.5; severe OSA (AHI ≥ 30/h): OR = 2.6, 95% CI: 1.1-6.2; and respiratory-related arousal index: ≥7.6/h, OR = 2.3, 95%CI: 1.1-4.7; but not measures of hypoxemia after adjustment for age, hypertension, diabetes, smoking, obesity, and NSAID use. There was no association of CKD with daytime sleepiness. In men with CKD, those with OSA were not significantly more likely to report symptoms (sleepiness, snoring, and apneas) or be identified with the STOP OSA screening questionnaire, compared to men without OSA., Conclusions: Predominantly mild CKD is associated with severe OSA and arousals. Further population studies examining the longitudinal relationship between CKD and OSA are warranted. Better methods are needed to identify OSA in CKD which may have few symptoms., (© Sleep Research Society 2016. Published by Oxford University Press on behalf of the Sleep Research Society. All rights reserved. For permissions, please e-mail journals.permissions@oup.com.)

A challenge for population health surveillance systems using telephone methodologies is to maintain representative estimates as response rates decrease. Raked weighting, rather than conventional poststratification methodologies, has been developed to improve representativeness of estimates produced from telephone-based surveillance systems by incorporating a wider range of sociodemographic variables using an iterative proportional fitting process. This study examines this alternative weighting methodology with the monthly South Australian population health surveillance system report of randomly selected people of all ages in 2013 (n = 7,193) using computer-assisted telephone interviewing. Poststratification weighting used age groups, sex, and area of residence. Raked weights included an additional 6 variables: dwelling status, number of people in household, country of birth, marital status, educational level, and highest employment status. Most prevalence estimates (e.g., diabetes and asthma) did not change when raked weights were applied. Estimates that changed by at least 2 percentage points (e.g., tobacco smoking and mental health conditions) were associated with socioeconomic circumstances, such as dwelling status, which were included in the raked-weighting methodology. Raking methodology has overcome, to some extent, nonresponse bias associated with the sampling methodology by incorporating lower socioeconomic groups and those who are routinely not participating in population surveys into the weighting formula., (© The Author 2015. Published by Oxford University Press on behalf of the Johns Hopkins Bloomberg School of Public Health. All rights reserved. For permissions, please e-mail: journals.permissions@oup.com.)

The recovery of EAU, a mouse model of endogenous human autoimmune uveitis, is marked with the emergence of autoantigen-specific regulatory immunity in the spleen that protects the mice from recurrence of EAU. This regulatory immunity is mediated by a melanocortin-driven suppressor APC that presents autoantigen and uses adenosine to activate an antigen-specific CD4(+) Tregs through the A2Ar. These cells are highly effective in suppressing uveitis, and they appear to be inducible Tregs. In this study, we determined whether they are inducible or natural Tregs and identified the dependent mechanism for the function of these post-EAU Tregs. The post-EAU spleen CD25(+)CD4(+) T cells were sorted for NRP-1 expression and transferred to recipient mice immunized for EAU. The sorted NRP-1(-), but not the NRP-1(+), Tregs suppressed EAU. These NRP-1(-) Tregs coexpress PD-1 and PD-L1. Treatment of naive APCs with α-MSH promoted a regulatory APC that induced CD25(+) CD4(+) Tregs in a CD73-dependent manner. These Tregs were PD-L1(+) PD-1(+) NRP-1(-) FOXP3(+) HELIOS(-) and suppressed EAU when transferred to recipient mice. In contrast, PD-1(-) T cells did not suppress EAU, indicating that PD-1 is necessary for the suppressive activity of iTregs. Moreover, these Tregs did not suppress effector T cells when the PD/-1/PD-L1 pathway was blocked. These results demonstrate that post-EAU Tregs are inducible Tregs, which use a PD-1/PD-L1 mechanism to suppress disease., (© Society for Leukocyte Biology.)

The Men Androgen Inflammation Lifestyle Environment and Stress (MAILES) Study was established in 2009 to investigate the associations of sex steroids, inflammation, environmental and psychosocial factors with cardio-metabolic disease risk in men. The study population consists of 2569 men from the harmonisation of two studies: all participants of the Florey Adelaide Male Ageing Study (FAMAS) and eligible male participants of the North West Adelaide Health Study (NWAHS). The cohort has so far participated in three stages of the MAILES Study: MAILES1 (FAMAS Wave 1, from 2002-2005, and NWAHS Wave 2, from 2004-2006); MAILES2 (FAMAS Wave 2, from 2007-2010, and NWAHS Wave 3, from 2008-2010); and MAILES3 (a computer-assisted telephone interview (CATI) survey of all participants in the study, conducted in 2010). Data have been collected on a comprehensive range of physical, psychosocial and demographic issues relating to a number of chronic conditions (including cardiovascular disease, diabetes, arthritis and mental health) and health-related risk factors (including obesity, blood pressure, smoking, diet, alcohol intake and inflammatory markers), as well as on current and past health status and medication., (Published by Oxford University Press on behalf of the International Epidemiological Association © The Author 2013; all rights reserved.)

Introduction: The progress and determinants of sexual dysfunction in middle-aged and elderly men remain unclear., Aim: To describe the incidence or remission and biopsychosocial predictors of erectile dysfunction (ED) and low sexual desire (SD)., Main Outcome Measures: Erectile function (International Index of Erectile Function) and sexual desire (Sexual Desire Inventory 2) were assessed at follow-up. Sociodemographic, lifestyle, and health-related factors were examined in multivariate models of ED and low SD., Methods: Data were collected from 810 randomly selected men residing in northern and western Adelaide, Australia, and aged 35-80 years at baseline, who made clinic visits 5 years apart., Results: At baseline, 23.2% (n = 123) of men had ED. ED incidence and remission were observed in 31.7% (n = 179) and 29.0% (n = 71) of eligible men, respectively. At baseline, 19.2% (n = 165) had low solitary sexual desire, and 6.0% (n = 50) had low dyadic sexual desire; incidence of low sexual desire occurred in 17.6% (n = 83) (solitary) and 8.3% (n = 51) (dyadic), while remission occurred in 15.4% (n = 68) (solitary) and 22.6% (n = 40) (dyadic) of men. In the final regression models, predictors of incident ED were higher age, lower income, higher abdominal fat mass, low alcohol intake, higher risk of obstructive sleep apnea (OSA) risk, voiding lower urinary tract symptoms (LUTS), depression, and diabetes. Predictors of ED remission were lower age, current employment, and absence of voiding LUTS, angina, diabetes, and dyslipidemia. Predictors of low dyadic SD incidence included higher age, never having been married, widowhood, being unemployed, being retired, insufficient physical activity, and low alcohol intake. Predictors of low dyadic SD remission were being married, not being widowed, higher income, lower abdominal fat mass, lower OSA risk, and higher plasma testosterone. Predictors of low solitary SD included never having been married, being unemployed, low alcohol intake, lower testosterone, storage LUTS, and hypertension. Predictors of low solitary SD remission were being married, being employed, higher income, higher physical activity, moderate alcohol intake, and depression., Conclusions: Sexual dysfunction in aging men is a dynamic disorder whose incidence and remission are predicted by a range of modifiable risk factors., (© 2014 International Society for Sexual Medicine.)

It is known that inoculation of antigen into the anterior chamber (a.c.) of a mouse eye induces a.c.-associated immune deviation (ACAID), which is mediated in part by antigen-specific local and peripheral tolerance to the inciting antigen. ACAID can also be induced in vivo by intravenous (i.v.) inoculation of ex-vivo-generated tolerogenic antigen-presenting cells (TolAPC). The purpose of this study was to test if in-vitro-generated retinal antigen-pulsed TolAPC suppressed established experimental autoimmune uveitis (EAU). Retinal antigen-pulsed TolAPC were injected i.v. into mice 7 days post-induction of EAU. We observed that retinal antigen-pulsed TolAPC suppressed the incidence and severity of the clinical expression of EAU and reduced the expression of associated inflammatory cytokines. Moreover, extract of whole retina efficiently replaced interphotoreceptor retinoid-binding protein (IRBP) in the preparation of TolAPC used to induce tolerance in EAU mice. Finally, the suppression of EAU could be transferred to a new set of EAU mice with CD8⁺ but not with CD4⁺ regulatory T cells (T(reg)). Retinal antigen-pulsed TolAPC suppressed ongoing EAU by inducing CD8⁺ T(reg) cells that, in turn, suppressed the effector activity of the IRBP-specific T cells and altered the clinical symptoms of autoimmune inflammation in the eye. The ability to use retinal extract for the antigen raises the possibility that retinal extract could be used to produce autologous TolAPC and then used as therapy in human uveitis., (© 2013 The Authors. Clinical and Experimental Immunology published by John Wiley & Sons Ltd on behalf of British Society. for Immunology.)

The evolutionarily conserved TGF-beta proteins are distributed ubiquitously throughout the body and have a role in almost every biological process. In immunity, TGF-beta has an important role in modulating immunity. Much is understood about the process of TGF-beta production as a latent molecule and of the consequences and the intercellular signaling of active TGF-beta binding to its receptors; however, there is little discussed between the production and activation of TGF-beta. This review focuses on what is understood about the biochemical and physiological processes of TGF-beta activation and identifies the gaps in understanding immune cell activation of TGF-beta. A mechanistic understanding of the process activating TGF-beta can lead to regulating multiple biological systems by enhancing or inhibiting TGF-beta activation.

The neuropeptide alpha-melanocyte-stimulating hormone (alpha-MSH) is a powerful suppressor of inflammation mediated by macrophages, which express at least two receptors, melanocortin 1 and 3 receptors (MC1r and MC3r) that bind alpha-MSH. Albeit, the anti-inflammatory activity of alpha-MSH has been well documented in macrophages, the mechanisms of alpha-MSH activity in macrophages are not clearly understood. This study is to investigate which of the MCr expressed on macrophages is associated with the immunosuppressive activities of alpha-MSH on LPS-stimulated macrophages. To address this question, we transfected RAW264.7 macrophage cells with MC1r small interfering (si)RNA, which specifically targets mouse MC1r mRNA. The diminution of MC1r mRNA expression was 82% at 24 h and 67% at 48 h after transfection. There was a significant loss in alpha-MSH suppression of NO generation and TNF-alpha production by MC1r siRNA-transfected macrophages stimulated with LPS. There was an equally diminished alpha-MSH suppression of LPS-stimulated intracellular activation of NF-kappaB and p38 phosphorylation. In addition, the diminishment of MC1r expression by siRNA transfection had no influence on MC3r expression and function in the macrophages. These findings demonstrate that alpha-MSH suppression of LPS-induced inflammatory activity in macrophages requires expression of MC1r. The results imply that although all of the MCr are G-coupled proteins, they may not necessarily function through the same intracellular pathways in macrophages.

We describe the creation of local immune privilege (IP) using retinal progenitor cells (RPCs) and biodegradable polymers. Murine RPCs were seeded on poly(lactic-coglycolic acid) polymers to generate composite grafts. Composites or RPCs alone were transplanted into allogeneic kidney capsules. Grafts survived at all time points, differentiating into neurons and astrocytes. Upon treatment with interferon gamma (IFNgamma), major histocompatibility complex antigens were upregulated. Although 10% of IFNgamma-treated RPC grafts survived 14 days, 66% of the IFNgamma-treated composites survived in part by producing immune suppressive factors transforming growth factor-beta2, Fas ligand, and indoleamine 2,3-dioxygenase. The composites were assayed for delayed-type hypersensitivity (DTH) by seeding composites with antigen-presenting cells incubated with ovalbumin. This resulted in suppression of ovalbumin-specific DTH, indicating that composite grafts consisting of biodegradable polymers and central nervous system progenitor cells can be used to generate local IP. This technology may be used to promote the survival of nonprivileged grafts (e.g., pancreas, liver, or skin). Disclosure of potential conflicts of interest is found at the end of this article.

T regulatory (Treg) cells have been studied for more than 30 years. Recently, changing technology and attitudes have led to new interest in T cell regulation of the immune responses. The eye is an immune-privileged site with unique mechanisms for the prevention of damaging immune inflammation. The eye fashions its Treg cells in novel ways to prevent immune inflammation locally and systemically. The purpose of this mini-review is to condense and summarize reports of Treg cells dependent on the eye in the context of the Treg literature in general.

The immune-privileged eye has the potential to induce regulatory immunity along with local mechanisms of immunosuppression. Rodent models of human autoimmune uveoretinitis [experimental autoimmune uveoretinitis (EAU)] recover without spontaneous recurrence of uveitis, which differs from uveitis in some humans. This raises the possibility that the mechanism of immune privilege in the rodent eye can reimpose itself during autoimmune uveoretinitis and re-establish tolerance to autoantigen. To investigate this possibility, we examined the spleens of EAU-recovered mice for regulatory immunity. We detected regulatory immunity when we adoptively transferred post-EAU spleen cells into other mice immunized for EAU. We could not detect this regulatory immunity in enucleated mice nor in naive mice. Moreover, unlike the mechanisms of anterior chamber-associated immune deviation, the suppression was only mediated by post-EAU CD4+ T cells, which required activation with autoantigen presented by post-EAU spleen antigen-presenting cells (APC). Our results demonstrate that when the immune-privileged ocular microenvironment recovers from an autoimmune response, it has influenced systemic immunity to retinal autoantigen by affecting APC and mediating induction of potential regulatory CD4+ T cells laying in wait in the post-EAU spleen for restimulation.

To evaluate the potential role of NK1.1 (CD161c) cells in autoimmune uveoretinitis, we treated experimental autoimmune uveoretinitis (EAU)-susceptible mice with anti-CD161c antibodies (PK136) to deplete natural killer (NK) cells. Injection of anti-CD161c antibodies deleted NK cells from the peripheral blood of EAU-susceptible mice. The T cell proliferative response against the ocular autoantigen K2 was not suppressed in mice treated with anti-CD161c antibody when compared with T cells from control mice. Although mice treated with anti-CD161c developed EAU, the clinical severity on days 17 and 19 after induction of EAU was significantly mild in anti-CD161c-treated mice compared with control mice. In addition, the histopathological severity of EAU was significantly milder in mice treated with anti-CD161c antibodies than controls 21 days after induction of EAU. Our results indicate that the severity of EAU is augmented by NK1.1(+) NK cells.

Recently, we have reported that the cytokines alpha-melanocyte-stimulating hormone (alpha-MSH) and transforming growth factor-beta2 (TGF-beta2) work in synergy to induce the activation of regulatory T (Treg) cells. When we used alpha-MSH and TGF-beta2 to generate ocular autoantigen-specific Treg cells and adoptively transferred them into mice susceptible to experimental autoimmune uveoretinitis (EAU), there was suppression in the incidence and severity of EAU. Specificity to a retinal autoantigen was required for the Treg cells to suppress EAU. When stimulated, these Treg cells produced TGF-beta1, and their production of interferon-gamma, interleukin (IL)-10, and IL-4 was suppressed. Also, the Treg cells are suppressed in their proliferative response. Our results demonstrate that alpha-MSH with TGF-beta2 induce Treg cells that can subdue a tissue-specific autoimmune response. This also promotes the possibility of using these immunomodulating cytokines to purposely induce antigen-specific Treg cells to prevent and suppress autoimmune disease.

Background: This study measured the prevalence of hearing impairment, and major demographic factors that influence the prevalence, in a representative South Australian adult population sample aged > or = 15 years., Methods: The study group was recruited from representative population surveys of South Australians. Participants in these surveys who reported a hearing disability were then recruited to an audiological study which measured air and bone conduction thresholds. In addition a sample of those people who reported no hearing disability were recruited to the audiological study., Results: The data reported in this study are the first in Australia to assess the prevalence of hearing impairment from a representative population survey using audiological methods. The data show that 16.6% of the South Australian population have a hearing impairment in the better ear at > or = 25 dBHTL and 22.2% in the worse ear at the same level. The results obtained in this representative sample compare well with those obtained in the British Study of Hearing, although some differences were observed., Conclusions: Overall, there are only a few studies worldwide that have audiologically assessed the impairment of hearing from a representative population sample. The overall prevalence of hearing impairment in Australia is similar to that found in Great Britain, although there are some differences between the estimates of severity of impairment and some sex differences. The corroboration of the two studies reinforces the status of hearing impairment as the most common disability of adulthood. The present study also showed that there are a large number of Australians who may benefit from a more systematic community-based rehabilitation programme including the fitting of hearing aids. Secondly, the study identified the need for health goals and targets for hearing to be based on an epidemiological approach to the problem.

The primary purpose of this study was to examine the effect of a 48-hour period of sleep deprivation on the performance of selected physical work tasks [30-45% of maximum oxygen consumption (VO2max)]. In addition, this study assessed the effect of continual performance of physical work during sleep deprivation on standardized physiological and psychological test scores. Nineteen male subjects performed six different physical tasks, designed to involve all major muscle groups, during a 48-hour period of sleep deprivation. Fourteen subjects served as sleep-deprivation controls. Performance on all physical work tasks decreased significantly. Neither sleep deprivation (SD) or sleep deprivation in conjunction with continuous physical work (SDW) had any effect on muscle contractile properties, anaerobic power measures or resting blood glucose and lactate concentrations. Only SD subjects demonstrated a decline in cardiorespiratory function. Self-selected walking pace decreased and perceived exertion increased significantly in the SDW group. Positive and negative mood scores were adversely affected in both groups, the total change being greatest in SD subjects. The results indicate that performance of physical work tasks requiring 30-45% VO2max declines significantly over a 48-hour period of sleep deprivation. However, maximal physiological function is not unduly compromised by either the work tasks in conjunction with sleep deprivation or by sleep deprivation alone.