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Biomedical subjects

J E Riggs

Publications and source records attributed to J E Riggs.

At least 19 recordsLinked to original sources
PubMed1995

Radiation-induced apoptosis is differentially regulated in primary B cells from normal mice and mice with the CBA/N X-linked immunodeficiency.

Normal B cells responsive to thymus independent-type 1 Ags (TI-1) are resistant to low doses of ionizing radiation in vivo (200-300 cGy), compared with TI-1 responsive B cells of mice with the CBA/N X-linked immunodeficiency (xid). This difference in radiosensitivity is an intrinsic B cell property; normal B cells adoptively transferred into xid mice remain TI-1-responsive after irradiation in situ. Because irradiation induces programmed cell death (PCD) in lymphocytes, we determined whether PCD were regulated differently in normal and xid B cells. B cells isolated immediately after irradiation from normal or xid donors when cultured without stimulators became apoptotic with the same kinetics and to the same extent, showing that apoptosis was induced equally in both populations. Apoptosis could be suppressed and mitogenesis could be induced frequently, however, if irradiated B cells were cultured with B cell activators. When activators using separate signal transduction pathways were compared, a hierarchy of efficiency at effecting apoptosis rescue was observed, and activators used singly without effect could synergize to protect. xid B cells were more resistant to rescue than normal B cells unless PMA was used as a stimulant. Although the mechanism of activator-induced rescue was not established, selective overexpression of a bcl-2 transgene rendered xid B cells radioresistant. The data suggest that a signal(s) delivered to irradiated B cells in the in vivo microenvironment suppresses apoptosis and that xid B cells and a radiosensitive subpopulation of normal B cells are refractory to this signal(s).

Animals↗
PubMed1995

Increasing multiple myeloma mortality rates in the elderly: demonstration of increasing dependency with increasing age upon age group population size.

Multiple myeloma mortality rates in the elderly are increasing. Using published United States mortality data, annual age-specific multiple myeloma mortality rates from 1968 to 1989 were determined for age groups over age 60 and compared to corresponding annual age group population sizes. Rising multiple myeloma mortality rates among the elderly in the United States from 1968 to 1989 were increasingly dependent, with increasing age, upon increasing age group population size. This finding suggests that differential survival, and its effect upon the surviving gene pool in an aging population, may account for observed increasing multiple myeloma mortality rates in recent successive elderly cohorts. A similar conclusion regarding increasing multiple myeloma mortality rates in the elderly has been derived using the Strehler-Mildvan modification of the Gompertz relationship.

Age Distribution↗
PubMed1995

Increasing multiple myeloma mortality among the elderly: a manifestation of aging and differential survival.

Increasing multiple myeloma incidence and mortality among the elderly in industrialized nations has been attributed to associated environmental carcinogens. Age-specific multiple myeloma mortality rates in the United States from 1968 to 1989 were analyzed using the Strehler-Mildvan modification of the Gompertz relationship between aging and mortality. The results suggest that worsening environmental influences are not responsible for increasing multiple myeloma mortality among the elderly. Differential survival, a concept originally popularized by Charles Darwin, and its effect upon the surviving gene pool in an aging population is an alternative explanation for increasing multiple myeloma incidence and mortality in the elderly.

Adult↗
PubMed1995

Rising primary malignant brain tumor mortality in the elderly. A manifestation of differential survival.

BACKGROUND: Increasing primary malignant brain tumor mortality among the elderly in developed countries over the past three decades has been attributed to improved diagnostic techniques and increased environmental carcinogens. OBJECTIVE: To demonstrate that rising primary malignant brain tumor mortality among the elderly can be accounted for by differential survival. DATA SOURCE: Published United States mortality data from the National Center for Health Statistics, 1962 to 1989. MEASURES: Age-specific primary malignant brain tumor mortality rates were determined for the age groups of more than 60 years old and compared with the population size of these age groups. RESULTS: Increasing primary malignant brain tumor mortality rates among the oldest age groups in the United States from 1962 to 1989 were directly proportional to the increasing population size of these age groups. CONCLUSIONS: Comparisons between age-specific mortality rates are generally considered valid since they are inherently age- and sex-matched. Moreover, age-specific mortality rates should not be related to population size. Rather than implying improved diagnosis or enhanced carcinogenesis, these results suggest that differential survival and its effect on the surviving gene pool in an aging population is an alternative explanation for the observed increase in primary malignant brain tumor mortality among the elderly.

Aged↗
PubMed1995

Rising ovarian cancer mortality in the elderly: a manifestation of differential survival.

Ovarian cancer mortality among the elderly in developed countries is increasing. Using published United States mortality data, annual age-specific ovarian cancer mortality rates from 1951 to 1989 were determined for the over-60 age groups and compared to corresponding annual age group population sizes. Rising ovarian cancer mortality rates among the elderly in the United States from 1951 to 1989 were increasingly dependent, with increasing age, upon increasing age group population size. These findings suggest that differential survival, and its effect upon the surviving gene pool in an aging population, may account for some of the observed increase in ovarian cancer mortality rates among recent successive elderly cohorts.

Age Distribution↗
PubMed1995

The murine autologous mixed lymphocyte response: distribution of stimulator cells.

Previous studies have shown that neonatal, but not adult, murine thymic T cells proliferate when co-cultured with syngeneic, adult splenic B cells. Evidence suggests that expansion of such self-reactive T cells precedes their clonal deletion or functional inactivation (anergy). This mechanism may be of particular significance for establishing peripheral (extrathymic) tolerance. In order to assess the autostimulatory capacity of B cells present in a variety of lymphoid tissues, neonatal T cells were cultured with Peyer's patch and peritoneal cavity cells. The results indicate that B cells in these tissues readily induce T cell proliferation. Evidence suggests that the B-1 B cell subpopulation is not obligatory for this process. Self-reactive T cells were evident in the spleen of young mice, substantiating a role for B cells in maintaining peripheral tolerance. The results suggest that B cells involved in this process are distributed in a variety of lymphoid organs.

Animals↗
PubMed1995

Increasing lung cancer mortality rates in the elderly: a manifestation of differential survival.

Lung cancer mortality rates in the elderly are increasing. Using published United States mortality data, annual age-specific lung cancer mortality rates from 1968 to 1989 were determined for age groups over age 50 and compared to corresponding annual age group population sizes. Rising lung cancer mortality rates among the elderly in the United States from 1968 to 1989 were increasingly dependent, with increasing age, upon increasing age group population size. This finding suggests that differential survival, and its effect upon the surviving gene pool in an aging population, may account for observed increasing lung cancer mortality rates in recent successive elderly cohorts. That is, increasing lung cancer mortality rates in the elderly may reflect changes in the genetic susceptibility of the surviving population rather than changes in environmental exposures.

Age Factors↗
PubMed1995

Acute confusional migraine: variant of transient global amnesia.

Acute confusional migraine in children and transient global amnesia in adults share a number of similar clinical manifestations. Acute confusional migraine in 6 children (mean age: 11.7 years; range: 7.5-17 years) was characterized by transient episodes of amnesia and acute confusion lasting 1-12 hours. Episodes were preceded by headache and vomiting in 4 patients. In 2 patients acute confusional migraine was the initial symptom. A history of preceding trivial head injury was reported in 3 patients and migraine in 4. Urine and serum drug screens were negative. Cerebral imaging studies and interictal electroencephalograms were normal. Ictal electroencephalograms in 3 patients revealed diffuse or bioccipital delta wave slowing. Recurrent episodes of acute confusional migraine occurred in 2 children during 1-3 years of follow-up. The clinical manifestations of acute confusional migraine in this series of children are similar to those reported in transient global amnesia. The similarity of the clinical manifestations of acute confusional migraine in children and transient global amnesia in adults suggests that these disorders may share a common pathophysiology.

Acute Disease↗
PubMed1995

Effect of carbamazepine and valproate on bone mineral density.

OBJECTIVE: To examine the effect of carbamazepine and valproate monotherapy on bone mineral density in children. METHODS: Axial (second, third, and fourth lumbar vertebrae) and appendicular (distal third of radius) bone mineral density was measured by dual-energy x-ray absorptiometry in 27 healthy children and 26 children with uncomplicated idiopathic epilepsy treated with either carbamazepine (n = 13) or valproate (n = 13) for more than 18 months. Control subjects and patients were similar with respect to age, race (all white), and geographic area, and had no dietary restrictions, neurologic impairment, or physical handicaps. RESULTS: Subjects were seizure-free for more than 6 months on a regimen of carbamazepine or valproate therapy, and had mean serum trough levels of 6.88 +/- 2 micrograms/ml and 72.04 +/- 45.6 micrograms/ml, respectively. Dietary calcium intake was similar in control and treated groups. After correction for gender and age, children treated with valproate had a 14% (p = 0.003) and 10% (p = 0.005) reduction in bone mineral density at the axial and appendicular sites, respectively. The reduction in bone mineral density increased with the duration of valproate therapy. Carbamazepine did not significantly reduce bone mineral density. CONCLUSION: Valproate montherapy, but not carbamazepine therapy, significantly reduces axial and appendicular bone mineral density in children with idiopathic epilepsy and may increase their risk of osteoporotic fractures.

Absorptiometry, Photon↗
PubMed1995

Critical illness neuromuscular disease in children manifested as ventilatory dependence.

Four children with prolonged dependency on a ventilator were found to have reversible quadriparesis, muscle wasting, and hyporeflexia after 8 to 20 days of assisted ventilation for life-threatening sepsis or respiratory failure. Critical illness neuromuscular disease, which was recently recognized as a distinct clinical syndrome in adults, may also be manifested in children by prolonged ventilatory dependency.

Adolescent↗
PubMed1995

Trauma, axonal injury, and amyotrophic lateral sclerosis: a clinical correlate of a neuropharmacologic model.

Axonal injury induces cell death in selectively vulnerable motor neurons of immature animals. This extensively studied animal model of trauma-induced motor neuron death is being used to develop the theoretical basis for the therapeutic use of neurotrophic factors to "rescue" dying neurons in amyotrophic lateral sclerosis, Parkinson's disease, and Alzheimer's disease. Antecedent trauma has been implicated as a precipitating factor for amyotrophic lateral sclerosis in susceptible individuals. The animal model of trauma-induced motor neuron death provides support for the concept that motor neurons in individuals susceptible to amyotrophic lateral sclerosis may be selectively vulnerable to trauma producing axonal injury. The case histories of six young adult men who developed amyotrophic lateral sclerosis after trauma with axonal injury are presented.

Adult↗
PubMed1995

Differential involvement of the brain in neonatal asphyxia: a pathogenic explanation.

Multiple cystic lesions in brain parenchyma supplied by the anterior cerebral circulation is a recognized pattern of cerebral injury associated with hypoxic-ischemic encephalopathy in the term infant. This report presents a series of seven infants (gestational age, 39.3 +/- 2.8 weeks; range, 36 to 44 weeks) who developed multicystic encephalomalacia in the distribution of the anterior cerebral circulation after severe neonatal asphyxia. Cerebral imaging and pathologic studies demonstrate relative preservation of the cerebellum, brain stem, and cerebral structures supplied by the vertebrobasilar circulation. Compared to the vertebrobasilar vasculature, the anterior cerebral vessels in the term infant have dense sympathetic innervation. Asphyxia, a potent sympathetic stimulator, may induce vasoconstriction in the anterior circulation and differentially accentuate the effects of hypoxia/ischemia on cerebral tissue.

Asphyxia Neonatorum↗