Mortality decline in The Netherlands in the period 1850-1992: a turning point analysis

The primary visual cortex (V1) of primates is unique in that it is both the recipient of visual signals, arriving via parallel pathways (magnocellular [M], parvocellular [P], and koniocellular [K]) from the thalamus, and the source of several output streams to higher order visual areas. Within this scheme, output compartments of V1, such as the cytochrome oxidase (CO) rich blobs in cortical layer III, synthesize new output pathways appropriate for the next steps in visual analysis. Our chief aim in this study was to examine and compare the synaptic arrangements and neurochemistry of elements involving direct lateral geniculate nucleus (LGN) input from the K pathway with those involving indirect LGN input from the M and P pathways arriving from cortical layer IV. Geniculocortical K axons were labeled via iontophoretic injections of wheat germ agglutinin-horseradish peroxidase into the LGN and intracortical layer IV axons (indirect P and M pathways to the CO-blobs) were labeled by iontophoretic injections of Phaseolus vulgaris leucoagglutinin into layer IV. The neurochemical content of both pre- and postsynaptic profiles was identified by postembedding immunocytochemistry for gamma-amino butyric acid (GABA) and glutamate. Sizes of pre- and postsynaptic elements were quantified by using an image analysis system, BioQuant IV. Our chief finding is that K LGN axons and layer IV axons (indirect input from M and P pathways) exhibit different synaptic relationships to CO blob cells. Specifically, our results show that within the CO blobs: 1) all K cell axons contain glutamate, and the vast majority of layer IV axons contain glutamate with only 5% containing GABA; 2) K axons terminate mainly on dendritic spines of glutamatergic cells, while layer IV axons terminate mainly on dendritic shafts of glutamatergic cells; 3) K axons have larger boutons and contact larger postsynaptic dendrites, which suggests that they synapse closer to the cell body within the CO blobs than do layer IV axons. Taken together, these results suggest that each input pathway to the CO blobs uses a different strategy to contribute to the processing of visual information within these compartments.     

Refocusing the lens: epidemiologic transition theory, mortality differentials, and the AIDS pandemic

The epidemiologic transition theory presented first by Omran [Omram. A. R. (1971) The epidemiologic transition: a theory of the epidemiology of population change, Mildbank Quarterly 49(4), 509-538] was designed to explain global trends in the dynamic relationship between epidemiological phenomena and demographic change. This paper argues that universalizing this theory only partially serves to explain mortality declines over the last century and eclipses key epidemiologic differences between population subgroups based on socioeconomic status, race, and sex. This paper examines morbidity and mortality differentials between population subgroups and demonstrates important inconsistencies with the optimistic trends implied by the epidemiologic transition theory, an argument further developed using the HIV/AIDS pandemic as a case study. The paper argues that these differences should be brought from margins to center to present a more complex and comprehensive picture of how population subgroups experience epidemiologic transitions differently.     

Accuracy and completeness of the registration of childhood leukaemia in The Netherlands, 1989-1992

In the Netherlands, childhood leukaemia is recorded by the Dutch Childhood Leukaemia Study Group (DCLSG, set up in 1972) and by nine regional cancer registries which together form the Netherlands Cancer Registry (NCR, set up in 1989). The data files from the incidence years 1989-1992 of the two registries were linked in order to evaluate accuracy and completeness and to calculate and equalise the incidence rates for childhood leukaemia in The Netherlands. Unlinked records or records with disagreements (birth date, sex, type of leukaemia and incidence date) were checked by the DCLSG and by the regional cancer registries. The DCLSG recorded 431 cases of childhood leukaemia, while the NCR recorded 434 cases. After record linkage and review of the cases, it was concluded the 445 records should have been recorded as childhood leukaemia. The NCR had recorded 425 of the 445 correct cases (95.5%), but had missed 20 cases (4.5%). The DCLSG had recorded 431 of the 445 correct cases (96.9%) and had missed 14 cases (3.1%). In addition, the NCR had recorded 9 cases incorrectly as childhood leukaemia. Part of the disagreement was caused by differences in coding rules (definition of non-Hodgkin's lymphoma (NHL) and the myelodysplastic syndrome versus leukaemia). It could be concluded that the quality and completeness of the two registries was very high. Regular comparison of the recorded data will help to reveal the inherently problematic disagreement between definitions and coding.     

National trends in the mortality of children with sickle cell disease, 1968 through 1992

OBJECTIVES: This paper describes national trends in mortality of children with sickle cell disease and the settings in which death occurred. METHODS: United States death certificate data from 1968 through 1992 were used to calculate mortality rates of Black children with sickle cell disease 1 to 14 years old. Deaths from trauma, congenital anomalies, and perinatal conditions were excluded. RESULTS: Between 1968 and 1992, mortality rates of Black children with sickle cell disease decreased 41% for 1- to 4-year-olds, 47% for 5- to 9-year-olds, and 53% for 10- to 14-year-olds. During 1986 through 1992, children who died before hospital admission accounted for 41% of deaths among 1- to 4-year-olds, 27% among 5- to 9-year-olds, and 12% among 10- to 14-year-olds. CONCLUSIONS: Survival of Black children with sickle cell disease has improved markedly since 1968. A substantial proportion of deaths continue to occur prior to hospital admission. Trends in sickle cell mortality can be monitored inexpensively with death-certificate data.     

Worldwide trends in suicide mortality, 1955-1989

Expression of keratin K5 (and K14) in multilayered epithelia occurs predominantly in the basal layer of proliferating keratinocytes. When a keratinocyte becomes committed to terminal differentiation, it moves out of the basal layer towards the epithelial surface. As part of this program of terminal differentiation, the expression of K5 (and K14) is downregulated in suprabasal cells, and new pairs of differentiation-specific keratins are expressed. To define the cis-acting DNA sequences required for K5 cell-type- and differentiation-specific expression, chimeric gene fusions between portions of the bovine keratin K5 locus and the Escherichia coli lacZ gene were used to generate transgenic mice. In the genomic fragment consisting of 5.3 kb of 5' flanking sequences, 6.1 kb corresponding to the body of the gene and 4.5 kb of 3' flanking sequences, the subfragment extending from -5300 bp to +138 bp was the smaller region that directed lacZ expression to stratified epithelia in a manner analogous to the endogenous keratin K5. Proximal sequences from -1300 bp to +138 bp were inactive. We also determined the expression pattern of keratin K5 during mouse development using an antiserum specific for mouse keratin K5. Expression was first detected in ectodermal cells of 11.5 days postcoitum embryos, and from day 13.5 postcoitum onwards K5 was detected in the precursors of most epithelia and organs which express K5 at adult stages. This pattern was reproduced, with few differences, by the construct with sequences from -5300 bp to +138 bp fused to the lacZ gene. These findings identify sequences between -5.3 kb and -1.3 kb of the bovine K5 gene as being important for cell-type- and differentiation-specific gene expression both during mouse development and in the adult.     

Trends and patterns of mortality associated with birth defects and genetic diseases in the United States, 1979-1992: an analysis of multiple-cause mortality data

Contemporary information on the trends and patterns of mortality associated with birth defects and genetic diseases is lacking in the United States. To study these trends and patterns, we used the Multiple-Cause Mortality Files of the National Center for Health Statistics. From 1979 through 1992, 320,208 deaths in the United States were associated with birth defects and genetic diseases. The age-adjusted mortality rates for people with birth defects declined from about 8.2/100,000 in 1979 to about 6.7/100,000 in 1992, and the mortality rates for people with genetic diseases increased from 2.2/100,000 in 1979 to 2.5/100,000 in 1992. The mortality rate was higher among men than among women and higher among blacks than among whites or other races for both birth defect- and genetic disease-associated deaths. The rate among infants with birth defects was more than 25 times higher than that among other age groups. About half of the children whose deaths were associated with birth defects had cardiovascular system defects, 15% had central nervous system defects, and 12% had chromosomal defects. For deaths associated with genetic diseases, hereditary neurologic or storage disorders were the most common genetic diseases (38%), followed by metabolic disorders (21%), sickle cell and thalassemia (12%). The decline in the rate of mortality from birth defects in the United States probably reflects improvements in medical and surgical care and other factors. Most of the mortality associated with birth defects remains in the pediatric age group (less than 15 years old). The upward trend we detected for the deaths with genetic diseases was most likely related to improved recognition and reporting of some genetic diseases rather than to the increased prevalence.     

Daily mortality in Madrid community 1986-1992: relationship with meteorological variables

Spontaneous regression of cancer is reported in virtually all types of human cancer, although the greatest number of cases are reported in patients with neuroblastoma, renal cell carcinoma, malignant melanoma and lymhomas/leukemias. Study of patients with these diseases has provided most of the data regarding mechanisms of spontaneous regression. Mechanisms proposed for spontaneous regression of human cancer include: immune mediation, tumor inhibition by growth factors and/or cytokines, induction of differentiation, hormonal mediation, elimination of a carcinogen, tumor necrosis and/or angiogenesis inhibition, psychologic factors, apoptosis and epigenetic mechanisms. Clinical observations and laboratory studies support these concepts to a variable extent. The induction of spontaneous regression may involve multiple mechanisms in some cases although the end result is likely to be either differentiation or cell death. Elucidation of the process of spontaneous regression offers the possibility of improved methods of treating and preventing cancer.     

Latent variable analyses of age trends of cognition in the Health and Retirement Study, 1992-2004.

The present study was conducted to better describe age trends in cognition among older adults in the longitudinal Health and Retirement Study (HRS) from 1992 to 2004 (N = 17,000). The authors used contemporary latent variable models to organize this information in terms of both cross-sectional and longitudinal inferences about age and cognition. Common factor analysis results yielded evidence for at least 2 common factors, labeled Episodic Memory and Mental Status, largely separable from vocabulary. Latent path models with these common factors were based on demographic characteristics. Multilevel models of factorial invariance over age indicated that at least 2 common factors were needed. Latent curve models of episodic memory were based on age at testing and showed substantial age differences and age changes, including impacts due to retesting as well as several time-invariant and time-varying predictors. (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Hemochromatosis-associated mortality in the United States from 1979 to 1992: an analysis of Multiple-Cause Mortality Data

BACKGROUND: Hemochromatosis, which can lead to serious chronic diseases resulting from iron overload, has an estimated prevalence of 50 to 80 cases per 10000 persons. However, little population-based information is available on the impact of hemochromatosis on morbidity and mortality. OBJECTIVE: To evaluate trends over 14 years in deaths and medical conditions associated with hemochromatosis in the United States. DESIGN: We searched Multiple-Cause Mortality Files compiled by the National Center for Health Statistics for the years 1979 to 1992 for all records listing hemochromatosis. We used these data to calculate age-adjusted and age-specific mortality rates, identify medical conditions associated with a known diagnosis of hemochromatosis at death, and calculate proportionate mortality ratios for these medical conditions. RESULTS: The listing of hemochromatosis on death certificates increased 60% from 1979 to 1992. Decedents with hemochromatosis were 23, 13, and 5 times more likely to have liver neoplasms, liver disease, and cardiomyopathy, respectively, than were decedents without hemochromatosis. Conversely, decedents with liver neoplasms, liver disease, and cardiomyopathy were 26, 14, and 5 times more likely, respectively, to have hemochromatosis than were decedents without these conditions. Hemochromatosis was 82 times more likely in persons with the combination of liver neoplasms and diabetes and 43 times more likely in those with the combination of liver disease and diabetes than in those without these conditions. CONCLUSIONS: Comparison of the reported prevalence of hemochromatosis among decedents with estimates of prevalence in the general U.S. population suggests that either the penetrance or the recognition of hemochromatosis, or both, is low. Nevertheless, substantial mortality resulting from liver disease, liver neoplasms, cardiomyopathy, and a combination of liver disease and diabetes in patients with hemochromatosis argues for the improved diagnosis and treatment of hemochromatosis in persons with these conditions.     

Tuberculosis mortality in England and Wales during 1982-1992: its association with poverty, ethnicity and AIDS

A linear DNA with partial sequence redundancy can be recircularized in cells by either nonhomologous end joining (NEJ) or by homologous recombination (HR). We have studied the relative contributions of these processes in zygotes or early embryos of species that serve as model organisms for developmental genetics. Thus, we have microinjected a linearized plasmid substrate into zygotes of zebrafish (Danio rerio) or into the posterior end of Drosophila melanogaster early embryos before pole cell formation. Similar to the situation observed previously in Xenopus zygotes/early embryos, we detected a large preponderance of DNA-end joining over homologous recombination. A comparison of end-joined junctions revealed that from the three species tested, zebrafish introduced the least number of sequence distortions upon DNA-end joining, while Drosophila produced the largest deletions (average 14 bp) with occasional nucleotide patch insertions, reminiscent of the N nucleotides at V(D)J junctions in mammalian immune receptor genes. Double-strand gap repair by homologous sequences ('homologous recombination') involving a bimolecular reaction was readily detectable in both zebrafish and Drosophila. This involved specifically designed recombination substrates consisting of a mutagenized linear plasmid and DNA fragments carrying the wild-type sequence. Our results show that the basic machinery for homologous recombination is present at early developmental stages of these two genetic model organisms. However, it seems that for any experimental exploitation, such as targeted gene disruption, one would have to inhibit or bypass the overwhelming DNA-end joining activity.     

Birthweight-specific trends in perinatal mortality by hospital category in South Australia, 1985-1990

OBJECTIVE: To investigate differences by birthweight in risk of perinatal death between level 3 hospitals (which provide care for high risk pregnancies and neonatal intensive care) and other hospitals in South Australia, using perinatal data for the 1985-1990 period. DESIGN: Analysis of birthweight-specific trends in risk of perinatal death by hospital category for singleton births, adjusting for risk factors. SUBJECTS: 114 725 singleton births of at least 400 g birthweight (or at least 20 weeks' gestation) born in hospitals in the 1985-1990 period and notified to the perinatal data collection. MAIN OUTCOME MEASURE: The relative odds of a perinatal death, as opposed to a live birth which survived the neonatal period. RESULTS: Births at level 3 hospitals had a higher crude risk of perinatal death than those at other hospitals, but this was due to the higher frequency of low birthweights at level 3 hospitals. For birthweights under 2000 g, and especially for the very low birth-weights, there was a higher risk at non-level-3 than level 3 hospitals. There was also the unexpected finding that births at level 3 hospitals in the 2500-2999 g range had a comparatively high risk of perinatal death. There was little difference in risk for births of higher birthweight. CONCLUSIONS: The greatly reduced risk of perinatal death in level 3 hospitals for babies with birthweights under 2000 g seems likely to be due to the specialist services in these hospitals. Further investigation is required to determine why babies in the 2500-2999 g range of birthweights had a comparatively high risk of perinatal death at these hospitals. This appears to be due, at least in part, to an excess contribution of deaths from congenital abnormalities. Also, it seems that the higher prevalence of complications in pregnancy in level 3 hospitals, and the transfers for induction of labour after intrauterine fetal death, would have made a contribution. These same factors may also have affected the risk in level 3 hospitals for higher birthweight births.     

The epidemiology of genitourinary fistulae in Kumasi, Ghana, 1977-1992

The aim of the study was to determine the clinical epidemiology of genitourinary fistulae as seen at Komfo Anokye Teaching Hospital in Kumasi, Ghana. A retrospective study was carried out from the hospital records and operative reports of all patients with genitourinary fistulae seen at Komfo Anokye Teaching Hospital between January 1977 and December 1992. Patient age, parity, type of fistula and cause of fistula were abstracted from the medical records. There were 164 cases of genitourinary fistula managed during the study period. There were 150 fistulae due to obstetric causes (91, 5%), the vast majority of which were due to prolonged obstructed labor (121 cases, 73.8% of all fistulae), with a minority related to complications of lower-segment cesarean section (14 cases, 8.5% of all fistulae). In 5 cases (3.1%) patients developed a rectovaginal fistula owing to perineal tears and prolonged obstructed labor. During this time period there were 157,449 deliveries, giving an obstetric fistula rate of 1 fistula per 1000 deliveries. Obstetric fistulae were most common at the extremes of reproductive age and parity Fourteen additional fistulae (8.5% of all cases) were due to gynecologic causes, most commonly from surgical injury occurring at the time of abdominal hysterectomy for leiomyomata uteri (12 cases, 7.3% of all fistulae). It was concluded that in Kumasi, Ghana, obstetric trauma from prolonged obstructed labor is the most common cause of genitourinary fistula formation. Such fistulae occur in older multiparous women as well in young primigravidae. Obstructed labour can, and does, occur in women who have previously undergone uneventful vaginal delivery. Birth attendants should be aware of that fact. Prompt referral for obstetric intervention should be made in obstructed labor, irrespective of the age and parity of the patient.     

Acute myocardial infarction case fatality, incidence and mortality rates in a population registry in Gerona, Spain, 1990-1992. REGICOR Investigators

BACKGROUND: Community-based registries provide the best approach to assessing the impact of myocardial infarction (MI) in a population. The objective of the present study was to determine MI mortality, incidence, attack rate and 28-day case fatality in the province of Gerona, Spain from 1990 to 1992. METHODS: Standardized methods were used to find, register and classify MI cases in that population (509628 inhabitants) as definite, possible and insufficient-data MI. RESULTS: Of the 1456 cases fulfilling eligibility criteria, 850 (58.4%) were classified as definite MI, 162 (11.1%) as fatal possible MI, 232 (15.9%) as no MI and 160 (11.0%) as fatal insufficient data. The 1990-1992 age-standardized incidence rates (first MI cases only) for definite and fatal possible MI were 140.8 per 100000 men and 20.4 per 100000 women, all aged 35-64 years; attack rates (first and recurrent MI cases) were 182.9 and 24.5, and mortality rates 46.4 and 5.8, respectively. Case fatality at 28 days was 27.4% and 19.9% in men and women, respectively, but women died later over that period. With respect to men, the age-adjusted risk among women of dying within 28 days post-MI was 1.26 (95% confidence interval [CI]: 0.94-1.69). CONCLUSIONS: Myocardial infarction, incidence, mortality rates and case fatality in Gerona are among the lowest in the world. Age-adjusted case fatality within 28 days is only marginally higher in women than in men, but fatal cases occur later within this period in women.     

Cancer incidence, mortality and survival: trends in four leading sites

Cancer mortality rates in the United States have stabilized in the past few years after rising for more than 50 years. Incidence and mortality rates for all cancers tend to be higher among men than women, among blacks than whites and among those over age 65. In 1994 cancer of the lung, prostate, breast, and colon/rectum (colorectal) will account for an estimated 57 percent of all new cancer cases and 55 percent of cancer deaths. Analysis of incidence, mortality and survival rates of these four major cancers indicate some encouraging trends. That is, even though age-adjusted incidence rates continue to increase, it appears that educational and screening efforts are having a positive influence on mortality rates. Lung cancer incidence has declined in recent years following a decrease in smoking among men that began some 20 years ago; evidence also indicates a start of a declining trend in their mortality from this disease, as well. Lung cancer incidence and mortality rates among women, however, continue to rise. In 1986 lung cancer became the leading cause of cancer deaths among women. Increased use and improved techniques of cancer detection for prostate, breast and colorectal cancers are resulting in larger numbers of these cancers being detected at early stages when they are more readily treatable. It is hoped that such activities will ultimately reduce mortality for these three major cancer sites.     

Forty years of evolution of mortality in Belgium and The Netherlands

Age adjusted mortality in Belgium (B) and The Netherlands (NL) was calculated from 5 yearly age-specific death rates between the ages 45-74 and 75-85+ years. Mortality was available in Belgium from 1954 to 1991 or 1994 (depending on the cause of death) and from 1950 to 1993 in The Netherlands. In the 45-74 years age class all-cause mortality decreased in B between 1955 and 1992 with 33% in men and 48% in women. In NL this was 11% and 40%, respectively. In the age class 75-85+ it was 21% and 37% in B, and 4% and 36% in NL, respectively. Since 1980 to the last available year there was a marked decrease in mortality in the age class 75-85+ years in men and women from B and no change in NL. Wallonia always had the highest mortality, followed by B, Flanders and NL. However, recently the observed mortality in Flanders was the lowest. Mortality trends, in both age classes and sexes, were obtained between 1980 to the last available year for 11 causes of death in men and 13 in women. Among 48 possible comparisons, 38 (79%) were in favor of B, 9 in favor of NL and 1 ex aequo. Life expectancy in 1992 was compared in the 15 EU countries. For both sexes together B ranked 8th, NL 3rd. The difference in life expectancy between the two countries was 3 year in 1967 and 1 year in 1992. Flanders ranked 5th (0.3 year lower than NL) and Wallonia 14th (2.2 years lower) when substituted for B in the EU. Portugal had the best and Denmark had the worst results between 1967 and 1992). Changes in life style-fat, salt, fruit and vegetable intake and smoking habits -which occurred since 1960 in B, its regions and in NI are consistent with the changes in mortality and life expectancy. Curative medicine and medical technology cannot explain the observed differences and trends.     

The placebo: Conceptual analysis of a construct in transition.

Suggests that the placebo in psychotherapy has retained the negative connotation of an inert "nuisance variable," a label that it originally incurred in the field of medicine. In addition, the transition toward more cognitive models of psychotherapy, particularly A. Bandura's (see record 1977-25933-001) theory of self-efficacy, has led to problems in defining the placebo within psychology. This transition has resulted in an awkward interface between certain preferred cognitive metaphors and the negative connotations of a presumably cognitive placebo construct. Suggestions have been made to dismiss the placebo construct from psychology and to do away with the use of true placebo controls in outcome research. The present analysis maintains that (a) the placebo can be adequately defined within psychology, (b) the negative connotation of the placebo label is largely undeserved, (c) the placebo retains a continuing conceptual and empirical utility for evaluating psychotherapy, and (d) the therapeutic efficacy of current therapies is well established even though they have not generally been shown to be more effective than nonspecific treatment. (29 ref) (PsycINFO Database Record (c) 2010 APA, all rights reserved)