Living the Good Life? Mortality and Hospital Utilization Patterns in the Old Order Amish

Lifespan increases observed in the United States and elsewhere throughout the developed world, have been attributed in part to improvements in medical care access and technology and to healthier lifestyles. To differentiate the relative contributions of these two factors, we have compared lifespan in the Old Order Amish (OOA), a population with historically low use of medical care, with that of Caucasian participants from the Framingham Heart Study (FHS), focusing on individuals who have reached at least age 30 years.Analyses were based on 2,108 OOA individuals from the Lancaster County, PA community born between 1890 and 1921 and 5,079 FHS participants born approximately the same time. Vital status was ascertained on 96.9% of the OOA cohort through 2011 and through systematic follow-up of the FHS cohort. The lifespan part of the study included an enlargement of the Anabaptist Genealogy Database to 539,822 individuals, which will be of use in other studies of the Amish. Mortality comparisons revealed that OOA men experienced better longevity (p<0.001) and OOA women comparable longevity than their FHS counterparts.We further documented all OOA hospital discharges in Lancaster County, PA during 2002–2004 and compared OOA discharge rates to Caucasian national rates obtained from the National Hospital Discharge Survey for the same time period. Both OOA men and women experienced markedly lower rates of hospital discharges than their non-Amish counterparts, despite the increased lifespan.We speculate that lifestyle factors may predispose the OOA to greater longevity and perhaps to lesser hospital use. Identifying these factors, which might include behaviors such as lesser tobacco use, greater physical activity, and/or enhanced community assimilation, and assessing their transferability to non-Amish communities may produce significant gains to the public health.     

Ten-Year Mortality and Cardiovascular Morbidity in the Finnish Diabetes Prevention Study—Secondary Analysis of the Randomized Trial

Background

The Finnish Diabetes Prevention Study (DPS) was a randomized controlled trial, which showed that it is possible to prevent type 2 diabetes by lifestyle changes. The aim of the present study was to examine whether the lifestyle intervention had an effect on the ten-year mortality and cardiovascular morbidity in the DPS participants originally randomized either into an intervention or control group. Furthermore, we compared these results with a population-based cohort comprising individuals of varying glucose tolerance states.

Methods and Findings

Middle-aged, overweight people with IGT (n = 522) were randomized into intensive intervention (including physical activity, weight reduction and dietary counseling), or control “mini-intervention” group. Median length of the intervention period was 4 years and the mean follow-up was 10.6 years. The population-based reference study cohort included 1881 individuals (1570 with normal glucose tolerance, 183 with IGT, 59 with screen-detected type 2 diabetes, 69 with previously known type 2 diabetes) with the mean follow-up of 13.8 years. Mortality and cardiovascular morbidity data were collected from the national Hospital Discharge Register and Causes of Death Register. Among the DPS participants who consented for register linkage (n = 505), total mortality (2.2 vs. 3.8 per 1000 person years, hazard ratio HR = 0.57, 95% CI 0.21–1.58) and cardiovascular morbidity (22.9 vs. 22.0 per 1000 person years, HR = 1.04, 95% CI 0.72–1.51) did not differ significantly between the intervention and control groups. Compared with the population-based cohort with impaired glucose tolerance, adjusted HRs were 0.21 (95% CI 0.09–0.52) and 0.39 (95% CI 0.20–0.79) for total mortality, and 0.89 (95% CI 0.62–1.27) and 0.87 (0.60–1.27) for cardiovascular morbidity in the intervention and control groups of the DPS, respectively. The risk of death in DPS combined cohort was markedly lower than in FINRISK IGT cohort (adjusted HR 0.30, 95% CI 0.17–0.54), but there was no significant difference in the risk of CVD (adjusted HR 0.88, 95% CI 0.64–1.21).

Conclusions

Lifestyle intervention among persons with IGT did not decrease cardiovascular morbidity during the first 10 years of follow-up. However, the statistical power may not be sufficient to detect small differences between the intervention and control groups. Low total mortality among participants of the DPS compared with individuals with IGT in the general population could be ascribed to a lower cardiovascular risk profile at baseline and regular follow-up.

Trial Registration

ClinicalTrials.gov {"type":"clinical-trial","attrs":{"text":"NCT00518167","term_id":"NCT00518167"}}NCT00518167     

Does P-Cresylglucuronide Have the Same Impact on Mortality as Other Protein-Bound Uremic Toxins?

Background

Uremic toxins are emerging as important, non-traditional cardiovascular risk factors in chronic kidney disease (CKD). P-cresol has been defined as a prototype protein-bound uremic toxin. Conjugation of p-cresol creates p-cresylsulfate (PCS) as the main metabolite and p-cresylglucuronide (PCG), at a markedly lower concentration. The objective of the present study was to evaluate serum PCG levels, determine the latter’s association with mortality and establish whether the various protein-bound uremic toxins (i.e. PCS, PCG and indoxylsulfate (IS)) differed in their ability to predict mortality.

Methodology/Principal Findings

We studied 139 patients (mean ± SD age: 67±12; males: 60%) at different CKD stages (34.5% at CKD stages 2–3, 33.5% at stage 4–5 and 32% at stage 5D). A recently developed high-performance liquid chromatography method was used to assay PCG concentrations. Total and free PCG levels increased with the severity of CKD. During the study period (mean duration: 779±185 days), 38 patients died. High free and total PCG levels were correlated with overall and cardiovascular mortality independently of well-known predictors of survival, such as age, vascular calcification, anemia, inflammation and (in predialysis patients) the estimated glomerular filtration rate. In the same cohort, free PCS levels and free IS levels were both correlated with mortality. Furthermore, the respective predictive powers of three Cox multivariate models (free PCS+other risk factors, free IS+other risk factors and free PCS+other risk factors) were quite similar - suggesting that an elevated PCG concentration has much the same impact on mortality as other uremic toxins (such as PCS or IS) do.

Conclusions

Although PCG is the minor metabolite of p-cresol, our study is the first to reveal its association with mortality. Furthermore, the free fraction of PCG appears to have much the same predictive power for mortality as PCS and IS do.     

Mortality trajectory analysis reveals the drivers of sex-specific epidemiology in natural wildlife–disease interactions

In animal populations, males are commonly more susceptible to disease-induced mortality than females. However, three competing mechanisms can cause this sex bias: weak males may simultaneously be more prone to exposure to infection and mortality; being ‘male’ may be an imperfect proxy for the underlying driver of disease-induced mortality; or males may experience increased severity of disease-induced effects compared with females. Here, we infer the drivers of sex-specific epidemiology by decomposing fixed mortality rates into mortality trajectories and comparing their parameters. We applied Bayesian survival trajectory analysis to a 22-year longitudinal study of a population of badgers (Meles meles) naturally infected with bovine tuberculosis (bTB). At the point of infection, infected male and female badgers had equal mortality risk, refuting the hypothesis that acquisition of infection occurs in males with coincidentally high mortality. Males and females exhibited similar levels of heterogeneity in mortality risk, refuting the hypothesis that maleness is only a proxy for disease susceptibility. Instead, sex differences were caused by a more rapid increase in male mortality rates following infection. Males are indeed more susceptible to bTB, probably due to immunological differences between the sexes. We recommend this mortality trajectory approach for the study of infection in animal populations.     

Mass Mortality of Adult Male Subantarctic Fur Seals: Are Alien Mice the Culprits?

Background

Mass mortalities of marine mammals due to infectious agents are increasingly reported. However, in contrast to previous die-offs, which were indiscriminate with respect to sex and age, here we report a land-based mass mortality of Subantarctic fur seals with apparent exclusivity to adult males. An infectious agent with a male-predilection is the most plausible explanation for this die-off. Although pathogens with gender-biased transmission and pathologies are unusual, rodents are known sources of male-biased infectious agents and the invasive Mus musculus house mouse, occurs in seal rookeries.

Methodology/ Principal Findings

Molecular screening for male-biased pathogens in this potential rodent reservoir host revealed the absence of Cardiovirus and Leptospirosis genomes in heart and kidney samples, respectively, but identified a novel Streptococcus species with 30% prevalence in mouse kidneys.

Conclusions/ Significance

Inter-species transmission through environmental contamination with this novel bacterium, whose congenerics display male-bias and have links to infirmity in seals and terrestrial mammals (including humans), highlights the need to further evaluate disease risks posed by alien invasive mice to native species, on this and other islands.     

Influenza Infectious Dose May Explain the High Mortality of the Second and Third Wave of 1918–1919 Influenza Pandemic

Background

It is widely accepted that the shift in case-fatality rate between waves during the 1918 influenza pandemic was due to a genetic change in the virus. In animal models, the infectious dose of influenza A virus was associated to the severity of disease which lead us to propose a new hypothesis. We propose that the increase in the case-fatality rate can be explained by the dynamics of disease and by a dose-dependent response mediated by the number of simultaneous contacts a susceptible person has with infectious ones.

Methods

We used a compartment model with seasonality, waning of immunity and a Holling type II function, to model simultaneous contacts between a susceptible person and infectious ones. In the model, infected persons having mild or severe illness depend both on the proportion of infectious persons in the population and on the level of simultaneous contacts between a susceptible and infectious persons. We further allowed for a high or low rate of waning immunity and volunteer isolation at different times of the epidemic.

Results

In all scenarios, case-fatality rate was low during the first wave (Spring) due to a decrease in the effective reproduction number. The case-fatality rate in the second wave (Autumn) depended on the ratio between the number of severe cases to the number of mild cases since, for each 1000 mild infections only 4 deaths occurred whereas for 1000 severe infections there were 20 deaths. A third wave (late Winter) was dependent on the rate for waning immunity or on the introduction of new susceptible persons in the community. If a group of persons became voluntarily isolated and returned to the community some days latter, new waves occurred. For a fixed number of infected persons the overall case-fatality rate decreased as the number of waves increased. This is explained by the lower proportion of infectious individuals in each wave that prevented an increase in the number of severe infections and thus of the case-fatality rate.

Conclusion

The increase on the proportion of infectious persons as a proxy for the increase of the infectious dose a susceptible person is exposed, as the epidemic develops, can explain the shift in case-fatality rate between waves during the 1918 influenza pandemic.     

Mortality from cardiovascular diseases in the German uranium miners cohort study, 1946–1998

An increased risk of cardiovascular diseases after exposure to low doses of ionizing radiation has been suggested among the atomic bomb survivors. Few and inconclusive results on this issue are available from miner studies. A positive correlation between coronary heart disease mortality and radon exposure has been reported in the Newfoundland fluorspar miners study, yet low statistical power due to small sample size was of concern. To get further insight into this controversial issue, data from the German uranium miners cohort study were used, which is by far the largest miner study up to date. The cohort includes 59,001 male subjects who were employed for at least six months between 1946 and 1989 at the former Wismut uranium company in Eastern Germany. Exposure to radon, long-lived radionuclides and external gamma radiation was estimated by using a detailed job-exposure matrix. About 16,598 cohort members were deceased until 31 December 1998, including 5,417 deaths from cardiovascular diseases. Linear Poisson regression models were used to estimate the excess relative risk (ERR) per unit of cumulative radiation exposure after adjusting for attained age and calendar period. No trend in risk of circulatory diseases with increasing cumulative exposure to either radon [ERR per 100 working level month: 0.0006; 95% confidence limit (CI): −0.004 to 0.006], external gamma radiation (ERR per Sv: −0.26, 95% CI: −0.6 to 0.05) or long-lived radionuclides (ERR per 100 kBqh/m³: −0.2, 95% CI: −0.5 to 0.06), respectively, was observed. This was also true for the sub-group heart disease and stroke. Our findings do not support an association between cardiovascular disease mortality and exposure to radiation among miners, yet low doses and uncontrolled confounding hamper interpretation.     

Mass Mortality of Coral Reef Ascidians Following the 1997/1998 El Niño Event

In April/May each year from 1995 to 2000, ascidians were sampled randomly with 35 1m² quadrats from three different reef habitats (intertidal reef tops, coastal reef walls and shallow-bank reefs) at four replicate localities (Praia do Forte, Itacimirim, Guarajuba and Abai) in northern Bahia (Brazil). As the sampling period included the 1997/1998 El Niño event, the most severe on record, for the first time these results allow a quantitative assessment of the impact of this major environmental stressor on the biodiversity of associated coral reef ascidians. Across all reef habitats, 22 ascidian species were recorded from three different orders (Aplousobranchia, Phlebobranchia and Stolidobranchia). After El Niño, all species showed significantly altered densities (ANOVA, F=602.90, p<0.0001); many species were absent from the reefs within 2 years of the El Niño period, but densities of Lissoclinum perforatum (all reefs) and Echinoclinum verrilli (subtidal reefs) increased significantly from 1998 onwards. Univariate and multivariate analyses confirmed that significant changes in assemblage composition had occurred. BIOENV analysis identified turbidity, mean temperature and cloud cover as the main factors best explaining these assemblage changes. Our results suggest that although the 1997/1998 El Niño had a differential effect on the species contributing to the ascidian assemblage of Brazilian coral reefs, most species disappeared and those remaining are likely to enhance reef degradation through their bioeroding activities.     

Arsenic Ingestion and Bladder Cancer Mortality—What Do the Dose-Response Relationships Suggest About Mechanism?

The Black–Foot Disease (BFD) endemic area of SW Taiwan has historically been the principal data source for assessing cancer risks from arsenic in drinking water in the United States, most recently in a 42–village ecological study. The data showed a discontinuity for bladder cancer risk at about 400 μg/L. A proposed explanation was that the arsenic–dependent bladder cancer risk was found only for those villages that were dependent on water from the artesian well aquifer (As > 350 μg/L and co–contamination with humic acids) and not for those villages receiving water from the shallow aquifer (As < 350 μg/L without humic acids). The humic acids were present from the algae that grew in the uncovered tanks holding the artesian water. The risk factors (slopes) developed from these subpopulations of the SW Taiwan study were applied to the data from an ecological study of median groundwater arsenic concentration and bladder cancer mortality in 133 U.S. counties dependent on groundwater to determine the slope most predictive of U.S. experience for bladder cancer mortality and arsenic ingestion (Lamm et al. 2004 Lamm, S H, Engel, AKruse, M B. 2004. Arsenic in drinking water and bladder cancer mortality in the United States: An analysis based on 133 U.S. counties and 30 years of observation.. J Occup Environ Med, 46(3): 298–306. [PUBMED][INFOTRIEVE][CSA][Crossref], [PubMed], [Web of Science ®] [Google Scholar]).The U.S. data excluded the SW Taiwan slope estimate derived from the artesian well–dependent subpopulation but were consistent with the slope estimate derived from the subpopulation using shallow aquifer water. Both the SW Taiwan data in the absence of high arsenic levels (< 350 μg/L) and humic acids and the U.S. 133–county data with As < 60 μg/L are consistent with no increased bladder cancer mortality risk from drinking water arsenic concentrations in the exposure range of observation. These analytic results are consistent with both co–carcinogenesis and high–exposure (hundreds of μ g/L As) dependence models of toxicological mode–of–action. These dose–response relationships should influence prioritization in the remediation of arsenic–contaminated drinking water supplies.     

BRONCHIAL ASTHMA—Patterns of Morbidity and Mortality in the United States, 1951-1959

On a nationwide basis, bronchial asthma occurs at the rate of 23 cases per 1,000 population. Young males develop bronchial asthma more readily and more severely than young females. Males dying from asthma outnumber females 2 to 1.Eight per cent of the asthmatic persons in the United States have not sought medical attention for this condition. Repeated attacks of severe bronchial asthma increase the likelihood of premature death.Approximately 6,000 deaths due to asthma occur annually in the United States, with a seasonal increase during the winter months. The estimated fatality rate of asthma in the general population is 1.5 deaths per 1,000 asthmatics.     

Is Exercise Protective Against Influenza-Associated Mortality?

Background

Little is known about the effect of physical exercise on influenza-associated mortality.

Methods and Findings

We collected information about exercise habits and other lifestyles, and socioeconomic and demographic status, the underlying cause of death of 24,656 adults (21% aged 30–64, 79% aged 65 or above) who died in 1998 in Hong Kong, and the weekly proportion of specimens positive for influenza A (H3N1 and H1N1) and B isolations during the same period. We assessed the excess risks (ER) of influenza-associated mortality due to all-natural causes, cardiovascular diseases, or respiratory disease among different levels of exercise: never/seldom (less than once per month), low/moderate (once per month to three times per week), and frequent (four times or more per week) by Poisson regression. We also assessed the differences in ER between exercise groups by case-only logistic regression. For all the mortality outcomes under study in relation to each 10% increase in weekly proportion of specimens positive for influenza A+B, never/seldom exercise (as reference) was associated with 5.8% to 8.5% excess risks (ER) of mortality (P<0.0001), while low/moderate exercise was associated with ER which were 4.2% to 6.4% lower than those of the reference (P<0.001 for all-natural causes; P = 0.001 for cardiovascular; and P = 0.07 for respiratory mortality). Frequent exercise was not different from the reference (change in ER −0.8% to 1.7%, P = 0.30 to 0.73).

Conclusion

When compared with never or seldom exercise, exercising at low to moderate frequency is beneficial with lower influenza-associated mortality.     

Myocardial Infarct Size and Mortality Depend on the Time of Day—A Large Multicenter Study

Background

Different studies have shown circadian variation of ischemic burden among patients with ST-Elevation Myocardial Infarction (STEMI), but with controversial results. The aim of this study was to analyze circadian variation of myocardial infarction size and in-hospital mortality in a large multicenter registry.

Methods

This retrospective, registry-based study was based on data from AMIS Plus, a large multicenter Swiss registry of patients who suffered myocardial infarction between 1999 and 2013. Peak creatine kinase (CK) was used as a proxy measure for myocardial infarction size. Associations between peak CK, in-hospital mortality, and the time of day at symptom onset were modelled using polynomial-harmonic regression methods.

Results

6,223 STEMI patients were admitted to 82 acute-care hospitals in Switzerland and treated with primary angioplasty within six hours of symptom onset. Only the 24-hour harmonic was significantly associated with peak CK (p = 0.0001). The maximum average peak CK value (2,315 U/L) was for patients with symptom onset at 23:00, whereas the minimum average (2,017 U/L) was for onset at 11:00. The amplitude of variation was 298 U/L. In addition, no correlation was observed between ischemic time and circadian peak CK variation. Of the 6,223 patients, 223 (3.58%) died during index hospitalization. Remarkably, only the 24-hour harmonic was significantly associated with in-hospital mortality. The risk of death from STEMI was highest for patients with symptom onset at 00:00 and lowest for those with onset at 12:00.

Discussion

As a part of this first large study of STEMI patients treated with primary angioplasty in Swiss hospitals, investigations confirmed a circadian pattern to both peak CK and in-hospital mortality which were independent of total ischemic time. Accordingly, this study proposes that symptom onset time be incorporated as a prognosis factor in patients with myocardial infarction.     

Mortality of an apex predator,the eagle owl bubo bubo,in Israel 2007–2021

Anthropogenic structures and installations in wild areas are known to directly and indirectly affect wildlife populations, especially apex predators such as Eagle Owls (Bubo bubo). To understand the situation at the national level we analyzed data collected by the Scientific Data Department of the Israel Nature and Parks Authority and the wildlife hospital at the Safari in Ramat Gan. We analyzed a total of 189 dead Eagle Owls during fifteen years, 2007–2021; 39.7% were electrocuted, 29.2% roadkill, 12.7% flew into fences/barbed wire, 3.8% drowned, and 14.9% died from other causes. The largest mortality of the Eagle Owls was detected in agricultural (34.92 %) and urban areas (31.74%). Also, the pylons identified as lethal should be prioritized and modified with appropriate insulators. Only a sincere effort on the part of the authorities will the continued electrocution of eagle owls and other avian wildlife be truncated.     

Hospitalization Rates and Post-Operative Mortality for Abdominal Aortic Aneurysm in Italy over the Period 2000–2011

Background

Recent studies have reported declines in incidence, prevalence and mortality for abdominal aortic aneurysms (AAAs) in various countries, but evidence from Mediterranean countries is lacking. The aim of this study is to examine the trend of hospitalization and post-operative mortality rates for AAAs in Italy during the period 2000–2011, taking into account the introduction of endovascular aneurysm repair (EVAR) in 1990s.

Methods

This retrospective cohort study was carried out in Emilia-Romagna, an Italian region with 4.5 million inhabitants. A total of 19,673 patients hospitalized for AAAs between 2000 and 2011, were identified from the hospital discharge records (HDR) database. Hospitalization rates, percentage of OSR and EVAR and 30-day mortality rates were calculated for unruptured (uAAAs) and ruptured AAAs (rAAAs).

Results

Adjusted hospitalization rates decreased on average by 2.9% per year for uAAAs and 3.2% for rAAAs (p<0.001). The temporal trend of 30-day mortality rates remained stable for both groups. The percentage of EVAR for uAAAs increased significantly from 2006 to 2011 (42.7 versus 60.9% respectively, mean change of 3.9% per year, p<0.001). No significant difference in mortality was found between OSR and EVAR for uAAAs and rAAAs.

Conclusions

The incidence and trend of hospitalization rates for rAAAs and uAAAs decreased significantly in the last decade, while 30-day mortality rates in operated patients remained stable. OSR continued to be the most common surgery in rAAAs, although the gap between OSR and EVAR recently declined. The EVAR technique became the preferred surgery for uAAAs since 2008.     

Epidemiological features of the first Unusual Mortality Event linked to cetacean morbillivirus in the South Atlantic (Brazil, 2017–2018)

Since the 1980s, cetacean morbillivirus (CeMV) has caused mass mortality events worldwide. However, no epizootics had been recorded in the South Atlantic, until an unusual mortality event (UME) linked to Guiana dolphin cetacean morbillivirus (GD-CeMV) began in Ilha Grande Bay, southeastern Brazil, in November 2017. In a five-month period, the UME spread to neighboring Sepetiba Bay and accounted for the death of at least 277 Guiana dolphins (Sotalia guianensis). Prevalence of morbillivirus positive dolphins, as estimated from RT-PCR diagnostics, was 92.3% (24/26) in Ilha Grande Bay and 91.9% (57/62) in Sepetiba Bay. Females had higher mortality rates during the UME (1.5:1), in contrast with historical mortality data from both bays that showed a 2:1 male to female death ratio. Calf mortality rates also increased in both bays. These results suggest that females and calves were more vulnerable to morbilliviral infection. Herein, we discuss possible explanations for such sex-biased death pattern during the UME and their implication for the conservation of endangered Guiana dolphins. We also speculate about the origin and spread of morbillivirus in the South Atlantic Ocean.     

Chronic Alcoholism-Mediated Impairment in the Medulla Oblongata: A Mechanism of Alcohol-Related Mortality in Traumatic Brain Injury?

Alcohol-related traumatic brain injury (TBI) is a common condition in medical and forensic practice, and results in high prehospital mortality. We investigated the mechanism of chronic alcoholism-related mortality by examining the effects of alcohol on the synapses of the medulla oblongata in a rat model of TBI. Seventy adult male Sprague–Dawley rats were randomly assigned to either ethanol (EtOH) group, EtOH-TBI group, or control groups (water group, water-TBI group). To establish chronic alcoholism model, rats in the EtOH group were given EtOH twice daily (4 g/kg for 2 weeks and 6 g/kg for another 2 weeks). The rats also received a minor strike on the occipital tuberosity with an iron pendulum. Histopathologic and ultrastructure changes and the numerical density of the synapses in the medulla oblongata were examined. Expression of postsynaptic density-95 (PSD-95) in the medulla oblongata was measured by ELISA. Compared with rats in the control group, rats in the chronic alcoholism group showed: (1) minor axonal degeneration; (2) a significant decrease in the numerical density of synapses (p < 0.01); and (3) compensatory increase in PSD-95 expression (p < 0.01). Rats in the EtOH-TBI group showed: (1) high mortality (50 %, p < 0.01); (2) inhibited respiration before death; (3) severe axonal injury; and (4) decrease in PSD-95 expression (p < 0.05). Chronic alcoholism induces significant synapse loss and axonal impairment in the medulla oblongata and renders the brain more susceptible to TBI. The combined effects of chronic alcoholism and TBI induce significant synapse and axon impairment and result in high mortality.     

Does Virus-Induced Lysis Contribute Significantly to Bacterial Mortality in the Oxygenated Sediment Layer of Shallow Oxbow Lakes?

Despite the recognition that viruses are ubiquitous components of aquatic ecosystems, the number of studies on viral abundance and the ecological role of viruses in sediments is scarce. In this investigation, the interactions between viruses and bacteria were studied in the oxygenated silty sediment layer of a mesotrophic oxbow lake. A long-term study (13 months) and a diel study revealed that viruses are a numerically important and dynamic component of the microbial community. The abundance and decay rates ranged from 4.3 × 10⁹ to 7.2 × 10⁹ particles ml of wet sediment⁻¹ and from undetectable to 22.2 × 10⁷ particles ml⁻¹ h⁻¹, respectively, and on average the values were 2 orders of magnitude higher than the values for the overlying water. In contrast to our expectations, viruses did not contribute significantly to the bacterial mortality in the sediment, since on average only 6% (range, 0 to 25%) of the bacterial secondary production was controlled by viruses. The low impact of viruses on the bacterial community may be associated with the quantitatively low viral burden that benthic bacteria have to cope with compared to the viral burden with which bacterial assemblages in the water column are confronted. The virus-to-bacterium ratio of the sediment varied between 0.9 and 3.2, compared to a range of 5.0 to 12.4 obtained for the water column. We speculate that despite high numbers of potential hosts, the possibility of encountering a host cell is limited by the physical conditions in the sediment, which is therefore not a favorable environment for viral proliferation. Our data suggest that viruses do not play an important role in the processing and transfer of bacterial carbon in the oxygenated sediment layer of the environment investigated.     

Mortality in Spinal Cord Injuries—Follow-up Report

The principal cause among 137 deaths in a series of 1,613 patients with traumatic spinal cord lesions treated at Veterans Administration Hospital, Long Beach, was renal disease attributable to the paralysis of the bladder and bladder sphincter and resultant genito-urinary tract infections. The second ranking cause was pulmonary disease. Before 1960 no deaths from cancer had occurred in this series, but between 1960 and 1962 three patients died of carcinoma of the bladder. It can be expected that as these patients reach higher age groups the incidence of neoplasms will increase.