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L LaRue

Publications and source records attributed to L LaRue.

8 recordsLinked to original sources
PubMed2001

Dialysis and disaster: San Francisco's dialysis community remembers the Loma Prieta earthquake. Interview by Susan L. Robertson.

Unlike many regions of the United States that live with seasonal disasters such as hurricanes, snow storms, or flooding from torrential rains, the greatest threat of natural disaster in California still comes from earthquakes (TransPacific Renal Network, 1998). This was proven on October 17, 1989 when the Loma Prieta earthquake rolled through northern California. Measured as 7.1 on the Richter scale, the quake's epicenter was located about 10 miles northeast of Santa Cruz along a segment of the San Andreas Fault near the town of Loma Prieta in the Santa Cruz Mountains. The impact, however, was felt throughout most of the northern portion of the state.

Adaptation, Psychological↗
PubMed1995

Safety and tolerability of the glutamate antagonist CGS 19755 (Selfotel) in patients with acute ischemic stroke. Results of a phase IIa randomized trial.

BACKGROUND AND PURPOSE: CGS 19755 is a competitive N-methyl-D-aspartate (NMDA) receptor antagonist that limits neuronal damage in animal stroke models. The objectives of this multicenter (7 centers), randomized, double-blind, placebo-controlled, ascending-dose phase IIa study were to evaluate the safety and tolerability of CGS 19755 and obtain pharmacokinetic and preliminary data on its efficacious dose range in patients treated within 12 hours of hemispheric ischemic stroke. METHODS: At each dose level, 6 patients were randomized to one or two intravenous bolus doses of CGS 19755, and 2 patients were randomized to placebo. An unblinded safety and monitoring committee-evaluated results at each dose before ascending to the next level. All patients at the first level (1 mg/kg) received two doses separated by 12 hours. The first 2 patients at 2 mg/kg received two doses, but adverse experiences occurred in both; subsequent patient groups received single doses of 2.0, 1.75, or 1.5 mg/kg. RESULTS: Adverse experiences (agitation, hallucinations, confusion, paranoia, and delirium) occurred in all 6 patients treated with 2 mg/kg, and in 3 of 5 at 1.75 mg/kg. Similar but milder adverse experiences were noted in 4 of 7 patients at 1.5 mg/kg and 1 of 6 patients at 1.0 mg/kg. Adverse experiences began between 20 minutes and 22 hours (mean, 8 hours) after treatment and lasted 2 to 60 hours (mean, 24 hours). Mortality was 1 of 8 in patients receiving placebo and 3 of 24 in treated patients. In treated survivors, median and mean percent improvement in National Institutes of Health Stroke Scale scores from baseline to terminal visit (mean, 86 days) was comparable at all doses, and 95% of treated patients had Barthel Index scores of > or = 70 at the terminal visit. CONCLUSIONS: We conclude that a single intravenous dose of 1.5 mg/kg CGS 19755 is safe and tolerable in patients with acute ischemic stroke. An efficacy trial is indicated.

Acute Disease↗
PubMed1989

Stroke in the Lehigh Valley: racial/ethnic differences.

We investigated black/white differences in stroke rate (standardized morbidity), severity, and subtype, and the relative frequencies of 5 primary risk factors (hypertension, diabetes, myocardial infarction, other heart diseases, and transient ischemic attack [TIA]) using the Lehigh Valley Stroke Register. Blacks had a statistically significant higher, age-adjusted rate of stroke than whites. We found no differences in stroke severity using our measures but blacks had a statistically higher proportion of lacunar stroke, while whites had a higher proportion of embolic stroke. There were no differences in proportions of thrombotic stroke or intracerebral hemorrhage. The relative frequencies of hypertension, myocardial infarction, other heart diseases, and diabetes were higher for blacks, while the relative frequency of TIA was higher for whites. These observations are consistent with other reports that blacks have a higher frequency of stroke and tend to have more small-vessel cerebrovascular pathology than whites.

Age Factors↗
PubMed1987

Does delay in acquiring childhood infection increase risk of multiple sclerosis?

Multiple sclerosis (MS) appears to be more common in technically advanced countries than in underdeveloped regions and migration from one area to another at a young age affects the risk of acquiring MS. One way of explaining both the peculiar frequency distribution and the effect of migration while young is to postulate that an infection early in life decreases the chance of central demyelination. However, no specific infection has been implicated consistently. Alternatively, an aberrant host response to infection in childhood might induce central demyelination. Thus, the aberrant host response could be age-dependent. In seeking associations between age of infection and risk of MS, we observed a direct relationship: where childhood diseases were acquired early in life, the frequency of MS in that population was low; where childhood diseases tended to occur nearer adolescence, MS frequency in that population was high. Since immune responsiveness to antigenic challenges matures through early adolescence, we reason that early infection might be protective and delay in acquiring childhood infections might increase the risk of developing MS. Indeed, in experimental models, the chance of inducing chronic relapsing central demyelination is increased by using adolescent rather than newborn or mature animals. In this paper, epidemiologic evidence showing the strong association between age of infection and risk of MS is presented.

Adolescent↗
PubMed1987

Does delay in acquiring childhood infection increase risk of multiple sclerosis?

Multiple sclerosis (MS) appears to be more common in technically advanced countries than in underdeveloped regions, and migration from one area to another at a young age affects the risk of acquiring MS. One way of explaining both the peculiar frequency distribution and the effect of migration while young is to postulate that an infection early in life decreases the chance of central demyelination. However, no specific infection has been implicated consistently. Alternatively, an aberrant host response to infection in childhood might induce central demyelination. Thus, the aberrant host response could be age-dependent. In seeking associations between age of infection and risk of MS, we observed a direct relationship: where childhood diseases were acquired early in life, the frequency of MS in that population was low; where childhood diseases tended to occur nearer adolescence, MS frequency in that population was high. Since immune responsiveness to antigenic challenges matures through early adolescence, we reason that early infection might be protective and that delay in acquiring childhood infections might increase the risk of developing MS. Indeed, in experimental models, the chance of inducing chronic relapsing central demyelination is increased by using adolescent rather than newborn or mature animals. In this paper, epidemiologic evidence showing the strong association between age of infection and risk of MS is presented.

Age Factors↗
PubMedDate not supplied

Acute stroke, hematocrit, and blood pressure.

A population-based study of the relation between hematocrit and stroke subtype was carried out among 2,077 individuals using the Lehigh Valley Stroke Register. This register identifies all stroke patients admitted to the 8 acute care hospitals serving the Lehigh Valley area of eastern Pennsylvania-western New Jersey. The mean hematocrit was higher in patients with lacunes than with thrombotic or embolic strokes (p = 0.02). However, when blood pressure was also considered the increase in hematocrit in patients with lacunar stroke was significant only when systolic hypertension (greater than or equal to 150 mm Hg) was also present (p = 0.029); no significant difference in hematocrit was found between stroke subtypes in normotensive individuals. Therefore, we cannot exclude the possibility that hypertension interacts with hematocrit in accounting for the observed association with lacunar infarcts. There was no trend for increased in-hospital mortality for stroke patients in either the low (less than or equal to 30, 30-36%) or high (greater than or equal to 47%) hematocrit groups.

Acute Disease↗