A scientist's guide for submitting data to ZFIN.

The Zebrafish Model Organism Database (ZFIN; zfin.org) serves as the central repository for genetic and genomic data produced using zebrafish (Danio rerio). Data in ZFIN are either manually curated from peer-reviewed publications or submitted directly to ZFIN from various data repositories. Data types currently supported include mutants, transgenic lines, DNA constructs, gene expression, phenotypes, antibodies, morpholinos, TALENs, CRISPRs, disease models, movies, and images. The rapidly changing methods of genomic science have increased the production of data that cannot readily be represented in standard journal publications. These large data sets require web-based presentation. As the central repository for zebrafish research data, it has become increasingly important for ZFIN to provide the zebrafish research community with support for their data sets and guidance on what is required to submit these data to ZFIN. Regardless of their volume, all data that are submitted for inclusion in ZFIN must include a minimum set of information that describes the data. The aim of this chapter is to identify data types that fit into the current ZFIN database and explain how to provide those data in the optimal format for integration. We identify the required and optional data elements, define jargon, and present tools and templates that can help with the acquisition and organization of data as they are being prepared for submission to ZFIN. This information will also appear in the ZFIN wiki, where it will be updated as our services evolve over time.

Suicide in countries and areas of the ESCAP region.

"In the ESCAP [Economic and Social Commission for Asia and the Pacific] region each year more than half a million people die by suicide and over 5 million attempt to kill themselves. This article collates available evidence about the incidence, age and sex patterns of suicide mortality in selected countries and areas of the region. It discusses cultural and legal attitudes towards suicide, as well as the social and health implications of the problem. It concludes by outlining some of the attempts that could be made at prevention both by governments and civil society."

A note on suicide in Russia, 1965-1993.

"Recently, the Centre for Demography and Human Ecology in Moscow in collaboration with the Institut National d'Etudes Demographiques in Paris undertook a reconstruction of registered deaths in individual republics of the former Soviet Union.... The present article extracts from the data set information on registered suicide mortality and reviews its trends and age and sex patterns. The link between alcoholism and suicide is strongly suggested."

Demographic and social profile of suicide mortality in Australia.

"In Australia, death rates from suicide of young and middle-aged men increased between the early 1970s and the early 1990s, whereas those of older men and of women declined markedly. The article identifies the possible extent of underreporting of suicides. The study then examines variations in the incidence of suicide by selected social characteristics of the population: marital status, social class and economic conditions, province of residence and country of birth. It closes by suggesting a tentative conceptual model linking social structures with levels of suicide." (SUMMARY IN ITA AND FRE)

[Suicide rates in Australia, 1971-1991]. / Sebevrazednost v Australii 1971-1991.

PIP: The author analyzes trends in suicide in Australia from 1971 to 1991. Aspects considered include sex distribution, marital status, native- or foreign-born, and cause of death. (SUMMARY IN ENG AND RUS)^ieng

Progress in demographic methodology.

"This paper examines developments in demographic methodology during the past decade or so. It focuses on methodological advances in the analysis of mortality of infants and young children, of adults, and on problems of mortality estimation in small populations. The other major areas reviewed here are related to the study of birth intervals, parity progression, proximate determinants of fertility, and the demography of the family. Concluding remarks relate the methodological issues to the information explosion in demography."

Suicide mortality in Australia, 1970-1991.

"This paper contains results of a study into changes in rates of suicide in Australia in the 1970s and 1980s. The study found that there was a significant divergence of suicide mortality rates between males and females, with male rates increasing in the last twenty years and female rates showing a general decline. The increase in male rates was highest at ages under 30 and over 80 years of age. The differences in rates between marital status groups have remained large. The study also analysed birthplace differentials in suicides and included some data from overseas countries for comparisons."

Immunocytochemical analysis of chromaffin cell proliferation in vitro.

The bromodeoxyuridine (BrdU) incorporation technique for immunocytochemical labeling of S-phase nuclei was optimized for the study of chromaffin cell proliferation. Sequential fixation in ethanol followed by paraformaldehyde, and the use of DNAse to render incorporated BrdU accessible to antibody, permitted permanent double staining for BrdU and tyrosine hydroxylase. The efficacy of the technique was demonstrated in microcultures of dissociated neonatal rat adrenal glands, in which chromaffin cells exhibited proliferative responses to nerve growth factor and fibroblast growth factor similar to those previously demonstrated by autoradiography. Growth factor responsiveness was observed in both serum-containing and serum-free medium.

Transition of adult mortality and causes of death in selected countries of Asia.

"The path of adult mortality in the... Asian countries that provide adequate data is examined and the diversity of mortality transitions as well as their vulnerability to temporary setbacks is documented.... In all the countries reviewed, a 'modernisation' of the cause of death structure occurred with infectious and parasitic diseases receding in importance and chronic and degenerative diseases taking up the leading position. Along with this change, [the authors find that] causes of death are becoming less relevant for the assessment of the health status of a population. The causes and the extent of temporary and permanent health impairments are more informative and appropriate for health policy strategies." (SUMMARY IN ITA)

Regulation of neurotensin content in adrenal medullary cells: comparison of PC12 cells to normal rat chromaffin cells in vitro.

Radioimmunoassay studies of cultures of PC12 pheochromocytoma cells have shown progressive increments in content and release of neurotensin in response to combinations of dexamethasone, nerve growth factor, activators of adenylate cyclase and lithium. We have studied the distribution of immunoreactive neurotensin by immunocytochemistry in cultures of PC12 cells and normal rat chromaffin cells, with two objectives: (i) to determine how changes measured by radioimmunoassay in extracts of PC12 cell populations are manifested at the level of individual cells and (ii) to determine whether normal chromaffin cells respond to combinations of agents similarly to PC12 cells. Staining for immunoreactive neurotensin is not identifiable in PC12 cells maintained in control medium or with any of the medium supplements alone. Approximately 3% of cells are stained after maintenance with dexamethasone plus nerve growth factor, verus 17% with dexamethasone plus nerve growth factor plus forskolin, and 33% with all four agents. This heterogeneity does not appear to result from clonal diversity, or to be cell cycle-dependent. Individual PC12 cells recruited to produce neurotensin in response to particular signals may, however, have passed a critical stage of differentiation toward a chromaffin cell, rather than neuronal phenotype before exposure to those signals. Staining for immunoreactive neurotensin is observed in up to 18% of normal chromaffin cells maintained with dexamethasone plus nerve growth factor, up to 45% with dexamethasone plus nerve growth factor plus forskolin, and up to 54% with all four agents. Proportions of cells stained under the various culture conditions are established before birth and in fetal cultures staining is confined for the most part to cells which do not undergo neuronal differentiation.(ABSTRACT TRUNCATED AT 250 WORDS)

A protein kinase inhibitor, staurosporine, mimics nerve growth factor induction of neurotensin/neuromedin N gene expression.

Nerve growth factor (NGF) cooperates with glucocorticoids, activators of adenylate cyclase, and lithium to induce the expression of teh gene encoding the neuropeptides neurotensin and neuromedin N (NT/N gene) in PC 12 pheochromocytoma cells. High level expression requires simultaneous treatment with three or all four inducers. To examine the mechanism underlying this complex synergism, we have examined the effects of protein kinase inhibitors and other agents which influence intracellular signal transduction on NT/N gene expression. Two structurally similar bacterial alkaloids, staurosporine and K-252a, inhibit several protein kinases in vitro, including protein kinase C and cyclic nucleotide-dependent kinases. K-252a has been reported to specifically inhibit the effects of NGF on PC12 pheochromocytoma cells. Surprisingly, staurosporine in combination with other inducers markedly potentiated NT/N gene expression. In contrast, K-252a had no effect on NT/N gene expression when added simultaneously with other inducers. Expression of the NT/N gene was also potentiated by the phorbol ester 12-O-tetradecanoylphorbol-13-acetate, which directly activates protein kinase C, and by bradykinin, which stimulates phosphatidylinositol turnover in PC12 cells, and these effects were not blocked by staurosporine. Staurosporine was generally more effective in stimulating NT/N gene expression when used in inducer combinations that did not include NGF. These results, taken together with recent evidence that staurosporine is also able to induce neurite outgrowth from PC12 cells, suggest that the effects of staurosporine and NGF may converge, in part, on a common intracellular target.

Mimicry and inhibition of nerve growth factor effects: interactions of staurosporine, forskolin, and K252a in PC12 cells and normal rat chromaffin cells in vitro.

The structurally similar compounds staurosporine and K252a are potent inhibitors of protein kinases. K252a has previously been reported to inhibit most or all of the effects of nerve growth factor (NGF) on PC12 pheochromocytoma cells, and staurosporine has been reported both to inhibit and to mimic NGF-induced neurite outgrowth from a PC12 cell subclone in a dose-dependent manner. We have studied the interactions of these agents with each other, with NGF, and with forskolin, an activator of adenylate cyclase, on the parent PC12 cell line and on normal neonatal and adult rat chromaffin cells. Staurosporine alone or in conjunction with forskolin induces outgrowth of short neurites from PC12 cells but does not substitute for NGF in promoting cell survival. It does not abolish NGF-induced neurite outgrowth but does reverse the effects of NGF on catecholamine synthesis. K252a abolishes NGF-induced neurite outgrowth but only partially decreases outgrowth induced by NGF plus forskolin. It does not inhibit neurite outgrowth produced by staurosporine or staurosporine plus forskolin. These findings with PC12 cells suggest that staurosporine might act downstream from K252a and NGF on components of one or more signal transduction pathways by which NGF selectively affects the expression of certain traits. Both neonatal and adult rat chromaffin cells show dramatic flattening and extension of filopodia in response to staurosporine, an observation suggesting that some of the same pathways might remain active in cells that do not exhibit a typical NGF response. Only a small amount of neurite outgrowth is observed, however, and only in neonatal cultures.(ABSTRACT TRUNCATED AT 250 WORDS)

Catecholamine-synthesizing enzymes and chromogranin proteins in drug-induced proliferative lesions of the rat adrenal medulla.

Both epinephrine (E) and norepinephrine (NE) cells in the rat adrenal medulla are able to proliferate in response to pharmacologic stimulation. However, previous biochemical studies have suggested that drug-induced or spontaneous pheochromocytomas in rats are almost invariably NE-producing. To resolve these apparently conflicting data, immunocytochemical techniques were utilized to establish functional profiles of adrenal medullary lesions classified as pheochromocytoma or nodular hyperplasia in rats treated chronically with a phosphodiesterase inhibitor which induced pheochromocytomas. Sixteen of 17 pheochromocytomas and all hyperplastic nodules stained positively for tyrosine hydroxylase and dopamine beta-hydroxylase, consistent with an ability to produce NE. No lesion of either type stained for phenylethanolamine N-methyltransferase, consistent with an inability to produce epinephrine. Lesions of both types showed variable staining for chromogranin proteins. The findings indicate that qualitative functional differences cannot be used to discriminate hyperplastic nodules from small pheochromocytomas in rats. Some lesions currently classified as hyperplastic nodules might in fact be small pheochromocytomas. Others might represent diffuse hyperplasia within pre-existing islands of NE-cells in a background of hyperplastic epinephrine-cells.

The use of cause-of-death statistics for health situation assessment: national and international experiences.

About 80 countries or areas regularly report detailed cause-of-death data to WHO based on the International Statistical Classification of Diseases, Injuries, and Causes of Death (ICD). These data refer to about 35% of all deaths estimated to occur in the world, although the actual coverage may be somewhat higher due to the representativeness of data-collection schemes in countries such as China. These data are systematically validated and documented by WHO before their dissemination, principally through publication in the World health statistics annual. This article describes the collection and use of these data by WHO for assessing the global and regional health situation, and for monitoring trends in health status. In addition, several issues in the use of mortality data and the ICD for national health situation assessment are discussed, including the need for documenting the quality and coverage of cause-of-death statistics, identifying biases and evaluating mortality trends.

Pharmacological stimulation of chromaffin cell proliferation in the adult adrenal medulla.

Many strains of rats develop adrenal medullary hyperplasia and/or neoplasia after chronic administration of a wide variety of pharmacologic agents. The same changes may occur spontaneously in the course of aging. Current evidence suggests that chromaffin cell proliferation in adult rats is regulated by a combination of hormonal and neurogenic signals. Drugs associated with adrenal medullary tumors might act directly or indirectly on the hypothalamic-endocrine axis or the autonomic nervous system to stimulate chromaffin cell proliferation through mechanisms which normally adjust cell number to meet physiological needs. The increased cell turnover rate might be a prelude to other events leading to neoplastic transformation.

Chromaffin cell proliferation in the adult rat adrenal medulla.

Epinephrine and norepinephrine-containing chromaffin cells proliferate in the adrenal glands of normal adult rats throughout life. Moreover, their rate of proliferation is markedly increased by short-term administration of reserpine, one of many agents which in long-term experiments are associated with the development of adrenal medullary tumors. Current data suggest that chromaffin cell proliferation in the adult rat adrenal is mediated by the interaction of neurogenic and hormonal signals. Reserpine is known to directly deplete catecholamine stores, and to reflexively increase the activity of the splanchnic nerve endings innervating the adrenal medulla to stimulate both secretion and synthesis of catecholamines and other secretory granule constituents. Its effect on chromaffin cell proliferation suggests that the same signals may regulate chromaffin cell number to meet physiological needs. The reserpine model might shed light on signal transduction mechanisms which normally promote or prevent proliferation of chromaffin cells and of other neuroendocrine cells during development or in adult life, and on ways in which such mechanisms are altered in the course of the development and progression of tumors. It also suggests the possibility that chromaffin cells might be propagated in vitro for use in basic biological studies or in transplants for the treatment of Parkinson's disease.

Infant and child mortality: the implications for fertility behaviour.

PIP: In developing countries, infant and child mortality affect fertility through biological or involuntary mechanisms operating through shortened breastfeeding, and more rapid return of ovulation following upon an infant death. Fertility is also affected through volitional responses of couples to perceived mortality levels in the community (insurance effect) or experience of earlier child loss (replacement effect) as well as through societal responses to high probability of child loss. In return, fertility affects infant and child mortality through birth to very young mothers, due to physiological immaturity of teenaged mothers and low birth-weight, as well as through birth to old mothers in high birth orders, due to maternal depletion syndrome. Trussel and Pebley estimated that the elimination of 4th and higher order births, along with the limitation of reproduction within the age of 20 to 34 years old, would reduce infant mortality by about 12%. A large number of studies show strong evidence that the timing and spacing of birth have a significant impact on both maternal and child health. According to Maine and McNamara (1985), who analysed data from 25 developing countries, if all children were born 2 years apart, 1/5 of infant deaths could be avoided. Mother's ill-health, maternal mortality, mother's malnutrition and its consequences in low quality breast milk and short breastfeeding, reduce sharply the new child's chances of survival. Many of these adverse biological and physiological conditions for childbearing can be compensated for by the provision of health care of high quality, including family planning, as well as education and good nutritional status of the mother and her children. Unfortunately, in many societies and for large segments of the population, such conditions are still a dream.^ieng

Recent trends in fertility and family formation.

"Australia's fertility has declined significantly since the 1950s, and has remained below the long-term replacement level since 1976. The current trend appears to be towards a further decline. This paper describes the patterns of the fertility decline in terms of age and parity of the mother, and the effect on recent fertility decline of the postponement of marriage and family formation. The implications of the continued decline in fertility on completed family size are studied by reference to fertility patterns of marriage cohorts."