Respiratory symptoms and bronchial responsiveness are related to dietary salt intake and urinary potassium excretion in male children

Six men were accidentally exposed to NO2 when they were changing a propeller using a gas burner in the poorly ventilated hold of a ship. All of them were admitted to hospital with shortness of breath and cough. Chest X-ray on admission revealed diffuse, patchy and infiltrative shadows, leading to the diagnosis of pulmonary edema in all five patients. Steroid therapy was effective and followed by a quick recovery in all patients. None developed third phase manifestations characterized pathologically by bronchiolitis obliterans.     

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.     

SPECT, CT, and MRI in head injury: acute abnormalities followed up at six months

We report a case of cervicofacial necrotizing fasciitis that developed after blepharoplasty, an occurrence that, to our knowledge, has not previously been reported in the medical literature. A patient who presented to our institution 3 days after undergoing blepharoplasty of the upper eyelid was diagnosed as having fulminant fasciitis involving extensive areas of the face, scalp, and neck. We review the case in detail and discuss clinical and radiological clues to diagnosis, surgical and medical management, wound care, and subsequent scar contracture. This case emphasizes the need for individualized, appropriate postoperative care and for an awareness of this rare, potentially fatal complication. Early recognition and aggressive treatment of cervicofacial fasciitis can arrest its rapid progression and prevent devastating sequelae.