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At least 19 recordsLinked to original sources
PubMed1989

Estimates of the maximum time required to originate life.

Fossils of the oldest microorganisms exist in 3.5 billion year old rocks and there is indirect evidence that life may have existed 3.8 billion years ago (3.8 Ga). Impacts able to destroy life or interrupt prebiotic chemistry may have occurred after 3.5 Ga. If large impactors vaporized the oceans, sterilized the planets, and interfered with the origination of life, life must have originated in the time interval between these impacts which increased with geologic time. Therefore, the maximum time required for the origination of life is the time that occurred between sterilizing impacts just before 3.8 Ga or 3.5 Ga, depending upon when life first appeared on Earth. If life first originated 3.5 Ga, and impacts with kinetic energies between 2 x 10(34) and 2 x 10(35) were able to vaporize the oceans, using the most probable impact flux, we find that the maximum time required to originate life would have been 67 to 133 million years (My). If life first originated 3.8 Ga, the maximum time to originate life was 2.5 to 11 My. Using a more conservative estimate for the flux of impacting objects before 3.8 Ga, we find a maximum time of 25 My for the same range of impactor kinetic energies. The impact model suggest that it is possible that life may have originated more than once.

Earth, Planet↗
PubMed2006

Early-life origins of the race gap in men's mortality.

Using a life course framework, we examine the early life origins of the race gap in men's all-cause mortality. Using the National Longitudinal Survey of Older Men (1966-1990), we evaluate major social pathways by which early life conditions differentiate the mortality experiences of blacks and whites. Our findings indicate that early life socioeconomic conditions, particularly parental occupation and family structure, explain part of the race gap in mortality. Black men's higher rates of death are associated with lower socioeconomic standing in early life and living in homes lacking both biological parents. However these effects operate indirectly through adult socioeconomic achievement processes, as education, family income, wealth, and occupational complexity statistically account for the race gap in men's mortality. Our findings suggest that policy interventions to eliminate race disparities in mortality and health should address both childhood and adult socioeconomic conditions.

Black or African American↗
PubMed2005

Pre-biotic stage of life origin under non-photosynthetic conditions.

Spontaneous assembling of a simplest bacterial cell even if all necessary molecules are present in a solution seems to be extremely rare event and from the scientific standpoint has to be considered as impossible. Therefore, a predecessor of a living cell has to be very simple for providing its self-assembling and at the same time it should be able of progressive increase in complexity. Now phase-separated particles, first of all micelles, are put forward as possible predecessors of living cell. According to the offered working concept only phase-separated particles possessing autocatalytic properties can be considered as predecessors of living cells. The first stage of evolution of these phase-separated autocatalytic systems is the appearance of pre-biotic metabolism providing synthesis of amphiphiles for formation of capsules of these systems. This synthesis is maintained by the energy of a base reaction being a component of a planet-chemical cycle. Catalytic system providing functioning of pre-biotic metabolism is based on multivariate oligomeric autocatalyst, which reproduces itself from monomers, penetrating the particles from the outside. Since the autocatalyst realizes random polymerization then a collection of other oligomers possessing different catalytic functions is produced. In the paper the functioning of multivariate oligomeric autocatalyst in flow reactor is analyzed.

Catalysis↗
PubMed1990

Impacts and the origin of life.

As living creatures, all of us have some interest in the question of how life originated. To some, the question is more religious than scientific; nonetheless, a small but dedicated group of scientists spend their careers trying to answer it from a rational standpoint. Logically, the question can be broken down into the three standard divisions of any mystery: When did life originate? Where did it originate? And how did it originate? Of these three sub-questions the last is by far the most difficult and I will make no attempt to address it here. I will however take a personal look at the two easier parts of the problem. In particular, I will outline my current view of the physical environment of the early Earth, and I will try to show how observations of other solar system bodies, especially our own Moon, provide clues as to when and where life could have originated.

Atmosphere↗
PubMed1997

Glucocorticoids, feto-placental 11 beta-hydroxysteroid dehydrogenase type 2, and the early life origins of adult disease.

Increasing human epidemiological data suggest that events that subtly retard intrauterine growth may determine common disorders, such as hypertension and non-insulin-dependent diabetes, in adult life. The underlying mechanisms are unknown. However, excessive fetal exposure to glucocorticoids retards growth and "programs" adult hypertension in rats. 11 beta-Hydroxysteroid dehydrogenase type 2 (11 beta-HSD2) catalyzes the rapid inactivation of cortisol and corticosterone to inert 11 keto-products. Normally, 11 beta-HSD2 in the placenta and some fetal tissues is thought to protect the fetus from excess maternal glucocorticoids. In both rats and humans there is considerable natural variation in placental 11 beta-HSD2, and enzyme activity correlates with birth weight. Moreover, inhibition of feto-placental 11 beta-HSD2 in the rat reduces birth weight and produces hypertensive and hyperglycaemic adult offspring, many months after prenatal treatment; effects are dependent upon intact maternal adrenals, suggesting a direct action on the fetus or placenta. Maternal protein restriction during pregnancy also produces hypertensive offspring and selectively attenuates placental 11 beta-HSD2 activity. These data suggest that feto-placental 11 beta-HSD2, by regulating fetal exposure to maternal glucocorticoids, crucially determines fetal growth and the programming of later disorders. Deficiency of the barrier to maternal glucocorticoids may represent a common pathway between the maternal environment and feto-placental programming of later disease. These data may, at least in part, explain the human observations linking early life events to the risk of subsequent disease.

11-beta-Hydroxysteroid Dehydrogenases↗
PubMed2004

Early life origins of insulin resistance and type 2 diabetes in India and other Asian countries.

There is a rapidly increasing epidemic of type 2 diabetes in India and other Asian countries. The thrifty genotype and the thrifty phenotype are two nonexclusive explanations. People in the Indian subcontinent have faced undernutrition for many generations, and Indian babies are among the smallest in the world. However, the diabetes epidemic is of recent origin, and diabetes is more common among urban than rural Indians despite the higher birth weight of urban babies. This suggests that postnatal factors must also contribute. Thus, a life-course model of evolution of insulin resistance and type 2 diabetes, incorporating fetal, postnatal and adult components, seems most appropriate. For a given BMI, Indians have a higher percentage of body fat and more visceral fat than members of other populations. This thin-fat phenotype is present at birth. Neonatal size and body composition are influenced by parental size, maternal food intake, physical activity and circulating concentrations of nutrients and metabolites (folate, glucose, triglycerides, cholesterol etc.). Maternal insulin resistance promotes transfer of nutrients to the fetus. Accelerated childhood growth is another risk factor for adiposity and insulin resistance, especially in children born small. Childhood growth seems to be more influenced by paternal genetic factors, whereas intrauterine growth is more influenced by maternal factors (intrauterine environment). Urban lifestyles, including poor diet and sedentary habits, promote further obesity, insulin resistance and type 2 diabetes. These factors may be amenable to correction. Prevention of type 2 diabetes must begin in utero and continue throughout the life course.

Adipose Tissue↗
PubMed1985

The organization of cell populations within lymph nodes: their origin, life history and functional relationships.

The normal lymph node comprises a superficial cortex, a deep cortex or paracortex and a medulla. In each of these regions there are three kinds of spaces: an intralymphatic space, an intravascular space and an extravascular space or interstitium. Both the vascular endothelium and the lymphatic endothelium are specialized in these different regions. The cell types in lymph nodes comprise lymphoid cells, accessory or non-lymphoid cells and stromal cells, and within these cell types a number of different sub-types can now be identified by means of enzyme- and immunocytochemistry. Based predominantly on experimental studies, the origin, migratory patterns, localization, inter-relationships and interactions between these various cells are reviewed.

Animals↗
PubMed2007

Manipulation of signaling to control allergic inflammation.

PURPOSE OF REVIEW: Inflammatory mediators produced from activated mast cells and T helper type 2 cells drive allergic inflammation. The pathways required for mast and T helper type 2 cell activation and the effects of their products are being defined in order to identify new therapeutics. We focus on recent findings on the chief inducer of mast cell activation, the IgE receptor-signaling cascade, and the development of new inhibitors of this pathway. We also summarize work that examines the molecular mechanisms utilized by the interleukin IL-4/13 receptors and characterizes therapeutic compounds that target these pathways. RECENT FINDINGS: The tyrosine kinases Lyn, Fyn and Syk have complex roles in IgE receptor signaling. Biochemical analysis and gene expression profiling have shed light on both the positive and negative functions of these proteins and establish additional connections with downstream pathways. Syk inhibitors were identified that may prove useful as antiinflammatory agents. Progress has been made in characterizing how IL-4/13 interact with their cognate receptors that will aid in the design of inhibitors of these interactions. SUMMARY: Recent studies have advanced our understanding of how the IgE receptor and IL-4/13 receptors function. This new knowledge may lead to the development of novel and highly specific inhibitors of allergic inflammation.

Animals↗
PubMed1991

Arteriolosclerosis of the human renal allograft: morphology, origin, life history and relationship to cyclosporine therapy.

In the decade 1979-1988, 658 biopsies were collected from 568 cadaveric renal allografts. In 118 grafts a non-proliferative insudative vasculopathy (IVA) was found in afferent vessels. Immunosuppression was based on azathioprine (AZA) or on cyclosporin A (CsA), from 1983. The prevalence and extent of IVA has increased significantly since 1984. Light microscopy showed fibrinoid and hyaline masses of varying extent; transmural insudative "knobs", intimal oedema with metachromasia, and microthrombosis were also seen with CsA. The ultrastructure of the insudates was unremarkable but CsA grafts displayed early oedema and hypergranulation of endothelial cells with a disarray of smooth muscle cell (SMC) microfibrils, and pronounced degenerative changes of SMC. Rebiopsy showed stationary IVA in AZA grafts and progression in one-half of CsA-treated patients. Nephrectomy specimens revealed, however, a marked predominance of late rejection endarteritis; in only 3 cases was IVA and/or microthrombosis the possible cause of nephrectomy. The mean donor age was higher in severe IVA in CsA grafts and the mean post-transplantation interval at the time of diagnosis of IVA was significantly shorter in CsA-treated patients. No important differences in cumulative graft survival were seen between grafts with absent, moderate or severe IVA. Unused cadaveric donors' kidneys of comparable age exhibited normal arterioles or a slight focal insudative or hyaline lesion.

Arteries↗
PubMed2004

Historic and early life origins of hypertension in Africans.

Cardiovascular disease (CVD) causes 12.4 million deaths annually, most (9.6 million) occurring in developing countries. Hypertension, the most common CVD, arises within the context of obesity, but the underlying mechanisms remain obscure. Obesity and salt intake are two important risk factors for hypertension and are the focus of this paper. Traditional African populations show a low prevalence of hypertension, but hypertension is more common in migrant African populations in the West than in other ethnic groups. One explanation is genetic, but no causative gene has been confidently identified. Nongenetic susceptibilities such as fetal programming are an alternative explanation. Hypothetically, fetal programming induced by transient stimuli permanently alters fetal structure and function at the cellular, organ and whole-body levels. Birth weight is inversely related to blood pressure and hypertension risk, suggesting that susceptibility to hypertension risk factors such as obesity and salt sensitivity are themselves programmed. In support of this hypothesis, obesity (especially central obesity) is also inversely related to size at birth. Likewise, salt sensitivity might derive from undernutrition in utero, reducing the nephron number and resetting the pressure-natriuresis curve rightward. However, no robust human data or evidence of enhanced salt sensitivity among African-origin populations exist. In the United States, blacks have a greater prevalence of low birth weight than whites, suggesting that the higher prevalence of hypertension among blacks is related to fetal programming. Nevertheless, we need to be scrupulous in ascribing risk to the myriad other confounders of this relationship, including environmental and behavioral correlates of ethnicity, before concluding that excess risk of hypertension in Africans is programmed in utero.

Africa↗
PubMed2005

Strong inverse association between height and suicide in a large cohort of Swedish men: evidence of early life origins of suicidal behavior?

OBJECTIVE: Previous studies have found associations between poor fetal and infant growth and the risk of suicide. The authors' goal was to investigate the association between height--a measure of childhood growth--and suicide risk. METHOD: The authors conducted a record linkage study of the birth, conscription, mortality, family, and census register data of 1,299,177 Swedish men followed from age 18 to a maximum of age 49. RESULTS: There were 3,075 suicides over an average follow-up period of 15 years. There was a strong inverse association between height and suicide risk. In fully adjusted models, a 5-cm increase in height was associated with a 9% decrease in suicide risk. CONCLUSIONS: The strong inverse association between height and suicide may signify the importance of childhood exposure in the etiology of adult mental disorder or reflect stigmatization or discrimination encountered by short men in their adult lives.

Adolescent↗