Thyroid doses resulting from the Ukraine Chernobyl accident--Part I: Dose estimates for the population of Kiev

In the context of the radiation exposure of the Ukrainian population resulting from the Chernobyl accident, the quantification of the thyroid doses due to iodine incorporation is of special interest. This first part of a series of planned publications deals with the dose and risk estimation for Kiev citizens. Although these doses are expected to be considerably lower than those for some other regions of Ukraine, the investigations started with this population because the quantification of the thyroid doses due to iodine incorporation is of special interest. This first part of a series of planned publications deals with the dose and risk estimation for Kiev citizens. Although these doses are expected to be considerably lower than those for some other regions of Ukraine, the investigations started with this population because of the availability of rather reliable measurements and because of the size of this population. The methods developed allowed the estimation of individual thyroid doses. The average values of individual thyroid doses for five age groups (birth years 1983-1986, 1979-1982, 1975-1978, 1971-1974, and < 1971) are 104, 62, 19, 18, and 41 mGy, respectively. The collective thyroid doses were estimated as 83 x 10(3) person-Gy for those born before 1971 and as 38 x 10(3) person-Gy for younger inhabitants. The numbers of expected thyroid cancers in the whole Kiev population are 66 and 130, respectively.     

Envelope glycoprotein gp120 of human immunodeficiency virus type 1 alters ion transport in astrocytes: implications for AIDS dementia complex

Infection by human immunodeficiency virus type 1 (HIV-1) is often complicated by a variety of neurological abnormalities. The most common clinical syndrome, termed acquired immunodeficiency syndrome (AIDS) dementia complex, presents as a subcortical dementia with cognitive, motor, and behavioral disturbances and is unique to HIV-1 infection. The pathogenesis of this syndrome is poorly understood but is believed to involve interactions among virally infected macrophages/microglia, astrocytes, and neurons. In this study, we show that exposure of primary rat and human astrocytes to heat-activated HIV-1 virions, or to eukaryotically expressed HIV-1 and HIV-2 envelope glycoproteins (gp120) stimulates amiloride-sensitive Na+/H+ antiport, potassium conductance, and glutamate efflux. These effects are blocked specifically by amiloride, an inhibitor of Na+/H+ antiport and by the selective removal of gp120 with immobilized monoclonal antibody. As a result of modulation of astrocytic function by gp120, the ensuing neuronal depolarization and glutamate exposure could activate both voltage-gated and N-methyl-D-aspartate-regulated Ca2+ channels, leading to increases in intraneuronal Ca2+ and neuronal death. These findings implicate the astrocyte directly in the pathogenesis of AIDS dementia complex.     

Genetics of programmed cell death in C. elegans: past, present and future

Genetic studies of the nematode Caenorhabditis elegans have defined a variety of single-gene mutations that have specific effects on programmed cell death. Analyses of the genes defined by these mutations have revealed that cell death is an active process that requires gene function in cells that die. Specific genes are required not only to cause cell death but also to protect cells from dying. Gene interaction studies have defined a genetic pathway for the execution phase of programmed cell death in C. elegans. Molecular and biochemical findings are consistent with the pathway proposed from these genetic studies and have also revealed that the protein products of certain cell-death genes interact directly. This pathway appears to be conserved among organisms as diverse as nematodes and humans. Important questions remain to be answered about programmed cell death in C. elegans. For example, how does a cell decide to die? How is cell death initiated? What are the mechanisms of action of the cell-death protector and killer genes? What genes lie downstream of the cell-death execution pathway? The conservation of the central cell-death pathway suggests that additional genetic analyses of programmed cell death in C. elegans will help answer these questions, not only for this nematode but also for other organisms, including ourselves.     

Using drug chronotherapy to wean patients from mechanical ventilation

Discontinuation of positive pressure mechanical ventilation results in decreased intrathoracic pressure. Although there has been extensive research into factors associated with weaning adults from mechanical ventilatory support, little attention has been paid to the role of left ventricular performance. Research also has not focused on interventions that might optimize ventricular performance. The purpose of this article is to explore the potential effect of cardiac dysfunction in weaning and the role of drug chronotherapy as a strategy to modify patients' responses to weaning from mechanical ventilatory support. Biophysical principles involved are reviewed, and the development of a chronotherapeutic intervention is described. Two case examples illustrate the use of drug chronotherapy during the weaning process.     

Isolation of porcine circovirus-like viruses from pigs with a wasting disease in the USA and Europe

Sinus pericranii is an anomalous extracranial vascular malformation that is in continuity with the intracranial dural venous sinuses. Five case reports, three congenital and two traumatic, are described. Clinical management, including evaluation, diagnosis, and treatment, is discussed. Awareness of this entity by plastic surgeons will allow for earlier diagnosis and appropriate surgical management, resulting in decreased risk of complications.