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Biomedical subjects

J Arden

Publications and source records attributed to J Arden.

10 recordsLinked to original sources
PubMed2001

Death due to bioterrorism-related inhalational anthrax: report of 2 patients.

On October 9, 2001, a letter containing anthrax spores was mailed from New Jersey to Washington, DC. The letter was processed at a major postal facility in Washington, DC, and opened in the Senate's Hart Office Building on October 15. Between October 19 and October 26, there were 5 cases of inhalational anthrax among postal workers who were employed at that major facility or who handled bulk mail originating from that facility. The cases of 2 postal workers who died of inhalational anthrax are reported here. Both patients had nonspecific prodromal illnesses. One patient developed predominantly gastrointestinal symptoms, including nausea, vomiting, and abdominal pain. The other patient had a "flulike" illness associated with myalgias and malaise. Both patients ultimately developed dyspnea, retrosternal chest pressure, and respiratory failure requiring mechanical ventilation. Leukocytosis and hemoconcentration were noted in both cases prior to death. Both patients had evidence of mediastinitis and extensive pulmonary infiltrates late in their course of illness. The durations of illness were 7 days and 5 days from onset of symptoms to death; both patients died within 24 hours of hospitalization. Without a clinician's high index of suspicion, the diagnosis of inhalational anthrax is difficult during nonspecific prodromal illness. Clinicians have an urgent need for prompt communication of vital epidemiologic information that could focus their diagnostic evaluation. Rapid diagnostic assays to distinguish more common infectious processes from agents of bioterrorism also could improve management strategies.

Abdominal Pain↗
PubMed1996

Basal phosphorylation of mu opioid receptor is agonist modulated and Ca2+-dependent.

The mu opioid receptor was shown to be phosphorylated at a basal rate in the absence of agonist, measured in permeabilized HEK293 cells transfected with an epitope tagged mu receptor (EE-mu) [Arden, J., Segredo, V., Wang, Z., Lameh, J. and Sadee, W. (1995) J. Neurochem. 65, 1636-1645]. In the present study, basal phosphorylation was found to be Ca2+ dependent; however, several inhibitors of protein kinase C and Ca2+-calmodulin dependent kinases failed to affect basal mu receptor phosphorylation. Thus, the basal mu receptor phosphorylating activity differed from the main kinases involved in receptor regulation. The general kinase inhibitor H7 (100 microM) suppressed basal mu receptor phosphorylation. Pretreatment with the agonist morphine, followed by drug removal, resulted in a sustained increase of basal mu receptor phosphorylation. The gradual agonist dependent modulation of basal mu receptor phosphorylation suggests a novel regulatory mechanism which may play a role in narcotic tolerance and dependence.

1-(5-Isoquinolinesulfonyl)-2-Methylpiperazine↗
PubMed1991

Childhood asthma mortality: the Brooklyn experience and a brief review.

Pediatric asthma mortality is a perplexing and increasingly serious problem. Although many possible etiologic factors have been suggested, clear relationships are yet to be delineated. In addition to reviewing the literature, we studied the clinical and pathologic features of 14 local pediatric asthma deaths that occurred over a 7-year period. Thirteen of 14 children were African-American. Nine of 14 children (64.3) were older than 10 years of age, and 11 of 14 (78.6) were males. Based on a history of clinical features, 10 of the 14 children were characterized as severe asthmatics. Despite the fact that the majority of the children were regarded as severe asthmatics, only 1 of 14 had been evaluated with pulmonary function testing, and only 2 of 14 were receiving corticosteroids. Furthermore, only 2 of 14 were regarded as having good medical follow-up for their asthma. Ten of 14 children died suddenly secondary to asthma. One child was possibly abusing sympathomimetic inhalers, and none had evidence of toxic serum levels of theophylline. Six of 14 children (all adolescents) who died suddenly were negative on urine toxicology screening for cocaine, heroin, etc. Pathologic findings available for 10 children revealed mainly mucus plugging of the airways and collapse of various segments of the lungs, as well as pneumonia and pneumothorax in one child. In this group of children with sudden deaths (except for one child with pneumothorax), no other cause of death could be found.

Adolescent↗
PubMed1988

The pharmacodynamics and pharmacokinetics of vecuronium in patients anesthetized with isoflurane with normal renal function or with renal failure.

The duration of action and the pharmacokinetics of vecuronium were compared in patients with and without renal function. Twenty patients were studied: 12 with renal failure who were to receive kidney transplants from cadaveric donors, and eight with normal renal function. After oral premedication with diazepam, 10 mg, anesthesia was induced with thiopental, 4 mg/kg iv, and maintained with the inhalation of 60% nitrous oxide and 0.9-1.1% isoflurane, end-tidal concentration, in 40% oxygen. The force of thumb adduction in response to supramaximal ulnar nerve stimulation was monitored and recorded. An intravenous bolus of vecuronium, 0.1 mg/kg, was administered after 15 min of a stable end-tidal isoflurane concentration, as measured by mass spectrometry. Venous blood was then sampled at frequent intervals for 4 h following the bolus. Vecuronium concentrations in plasma were quantified by a sensitive and specific gas chromatographic assay. Data were analyzed by nonlinear least squares regression and described by a two-compartment model. The duration of neuromuscular blockade was longer in patients with renal failure than in those with normal renal function. This increased duration may be related to both a decreased plasma clearance and a prolonged elimination half-life of vecuronium in the renal failure group.

Anesthesia, Inhalation↗