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J F Crocker

Publications and source records attributed to J F Crocker.

At least 55 records · Page 3Linked to original sources
PubMed1987

Pitfalls in the initial diagnosis of tyrosinemia: three case reports and a review of the literature.

The tyrosinemias are a complex and heterogeneous group of disorders in tyrosine catabolism that embrace a wide spectrum of clinical conditions, ranging from the benign neonatal variety to the severe hepatorenal form. Readily available diagnostic tests are too insensitive to distinguish between these variants, and more definitive but technically difficult tests can be performed rapidly in only a few centres. Effective management may therefore be compromised, due to the inability of obtaining a working diagnosis quickly. This report describes difficulties encountered with conventional testing in three patients. Analysis of whole blood delta-aminolevulinic acid dehydratase activity and determination of urinary inhibition activity against the enzyme were found to be rapid and reliable screening tests for hepatorenal or type I hereditary tyrosinemia. These procedures are recommended in the initial evaluation of undifferentiated tyrosinemic states.

Amino Acid Metabolism, Inborn Errors↗
PubMed1987

Polycystic kidney and liver disease and corticosterone changes in the cpk mouse.

Mice homozygous for the mutation cpk develop a lethal infantile polycystic kidney disease (PKD) and have abnormal elevations of corticosterone in the postnatal period. We examined the development of these elevated glucocorticoid levels in early life. The histological progression of a cystic lesion of the biliary ducts in older heterozygotes was also studied. Normal mice had low (less than 85 nmol/liter) or undetectable (less than 36 nmol/liter) levels from the sixth to twelfth day of life. Corticosterone levels were significantly higher in all homozygote (cpk/cpk) and some of the normal sibs, who were presumed to be heterozygote (cpk/+) mice compared to age-matched controls from day seven to 12. Corticosterone levels were similar from the fifteenth day. A significant proportion of adult obligate heterozygotes from breeding pairs were found to have focal areas of cystic dilatation of the biliary ducts, in the absence of any renal abnormality. The incidence of this lesion increased with age (10% at 150 days, 23% at 300 days, 29% at 450 days, 65% at greater than 450 days of age). The livers of homozygote mice dying in infancy, and control adult mice of the C57BL/6J background strain were free of cysts. The finding of hepatic cysts is reminiscent of adult type PKD. The cpk model thus supports the concept that the different forms of PKD may represent varying expression of a similar gene complex.

Animals↗
PubMed1986

Serum lipid abnormalities in a chemical/viral mouse model for Reye's syndrome.

Neonatal mice given nontoxic dermal applications of an industrial surfactant, Toximul MP8 (Tox), and subsequently infected with sublethal doses of mouse-adapted human Influenza B (Lee) virus (FluB) develop many of the biochemical features of Reye's Syndrome (RS). To determine whether these also include abnormal circulating lipid, we examined serum lipid profiles in the mouse model throughout the treatment course using Iatroscan-TH10. Following 10 days of exposure to surfactant, serum phospholipid and cholesterol levels were significantly reduced relative to control animals. These reductions were transient; however, four days following virus administration, significant differences in serum lipid were again evident. These abnormalities coincided and correlated with increased animal mortality. Animals that received combined Tox + virus treatment had significant decreases in serum total lipids relative to control animals, a reflection of a reduction in all lipid classes, including phospholipid, cholesterol, neutral glycerides (triglycerides plus diglycerides) and free fatty acids. Phospholipid (specifically phosphatidylcholine and lysophosphatidylcholine) and free fatty acid levels in the Tox + virus group were also significantly lower than those in animals that received virus alone. This study has demonstrated that suckling mice given chemical/viral treatment have the serum hypopanlipidemia but not the freefattyacidemia that are characteristic of RS.

Animals↗
PubMed1986

Biochemical and morphological characteristics of a mouse model of Reye's syndrome induced by the interaction of influenza B virus and a chemical emulsifier.

One theory of the etiology of Reye's syndrome is that environmental toxins predispose the child to react abnormally to virus infection. Influenza B is the most commonly implicated virus. Suckling mice were exposed to a surfactant, Toximul MP8, either by a single intraperitoneal injection or by repeated applications to the skin. At various times after exposure, the mice were infected intranasally with influenza B virus. Mice exposed to a combination of chemical and virus had a higher mortality rate than that of the control groups. Serum ammonia levels were elevated and the mitochondrial urea cycle enzyme, ornithine transcarbamylase, had reduced activity in the livers of mice exposed to Toximul and infected with virus. The hepatocyte cytoplasmic urea cycle enzyme concentrations were variable. Livers of the animals with "chronic" skin application of Toximul followed by virus infection showed mitochondrial swelling and breakdown of cristae. Those animals who received one intraperitoneal injection of Toximul and those infected with virus alone showed either negative or mild morphologic changes in the liver. We conclude that young mice exposed to a chemical emulsifier and subsequently to influenza B develop histomorphic and urea cycle changes, as well as hyperammonemia analogous to human Reye's syndrome.

Ammonia↗
PubMed1985

The comparative toxicity of vitamin D metabolites in the weanling mouse.

The potential toxicity of vitamin D, alpha-calcidol [1 alpha(OH)D3], and calcitriol [1,25(OH)2D3] was studied by administration of these compounds at three different doses to weanling C57BL/6J mice over a 4-week period. Drug effects on calcium were monitored by serum calcium and urine calcium/creatinine ratio determinations. Tests of renal function included serum creatinine, 24-h urine volume, urinary protein, and glucose excretion, and histological evaluation of renal tissue. At 2 weeks, serum calcium was significantly elevated in animals receiving the higher doses of alpha-calcidol (2.78 +/- 0.25 at 50 ng/kg and 3.45 +/- 0.13 at 250 ng/kg body wt vs 2.14 +/- 0.06 mmol/l in controls, respectively). A similar effect was seen in the urinary calcium/creatinine ratio but serum creatinine remained unchanged. By 4 weeks, all animals receiving alpha-calcidol had significantly higher serum calcium and urinary calcium/creatinine ratios than other groups. Severe nephrocalcinosis was observed in the high-dose alpha-calcidol group only. We conclude that alpha-calcidol is more toxic than calcitriol in the mouse and suggest that the degree of toxicity is correlated to the degree of hypercalcemia and to the vitamin D metabolite used.

Animals↗
PubMed1982

Is a compromised interferon response an etiologic factor in Reye's syndrome?

Young mice injected with sublethal doses of Toximul MP8, a typical commercial polyoxyethylene ether-based emulsifier, died more frequently when infected with encephalomyocarditis virus than did control mice. Lymphocytes taken from emulsifier-injected mice responded poorly to interferon induction, unlike lymphocytes from control animals. Interferon protected control mice against viral encephalomyocarditis, but such protection was not equally demonstrable in emulsifier-injected mice. These data suggest that the enhanced lethality of encephalomyocarditis virus in emulsifier-injected mice is associated with and perhaps caused by a compromised interferon response in these animals. Since these emulsifiers are commonly found in the environment in areas where forests are sprayed with pesticides, a group of children suffering from Reye's syndrome who lived in such areas was investigated. Blood samples were obtained from five children with influenza B-associated Reye's syndrome during their acute illness and during convalescence. Lymphocytes obtained from these samples and from peripheral blood samples from healthy children (controls) were induced to synthesize interferon by exposure to Newcastle disease virus. The lymphocytes from the convalescent patients and from the controls responded well to induction. However, the lymphocytes obtained from patients and from the controls responded well to induction. However, the lymphocytes obtained from patients during the acute phase of Reye's syndrome responded very poorly and produced significantly less interferon.

Acute Disease↗
PubMed1982

Reye's syndrome.

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Aflatoxins↗
PubMed1981

Reye's syndrome: a clinical review.

Reye's syndrome is a virus-associated biphasic disease that causes acute encephalopathy in infants and children. Epidemiologic and experimental data support the hypothesis that it is a multifactorial disease of modern civilization. Just as young patients seem to be recovering uneventfully from the first phase of the illness, usually a nonspecific viral-like illness such as a respiratory tract infection or gastroenteritis, the second phase, encephalopathy, starts unexpectedly, with vomiting and sensorial changes. Identifying the syndrome early ;in the second phase and referring the child to a specialized centre with the experience, staff and facilities to manage this phase has improved the numbers and neurologic condition of survivors, though the overall mortality is still about 20%. Therapy is primarily directed at facilitating adequate cerebral perfusion pressure.

Adolescent↗
PubMed1981

Identification of a toxic impurity in commercial diphenylamine.

The impurity in commercial diphenylamine which induces polycystic kidney disease in rats has been identified as N,N,N'-triphenyl-p-phenylenediamine. The structure of the compound was confirmed by mass and proton magnetic resonance spectrometry and by comparison with a synthetic standard prepared by the Ullman coupling of iodobenzene and p-phenylenediamine or N,N-diphenyl-p-phenylenediamine. Laboratory studies with highly purified diphenylamine indicated that N,N,N'-triphenyl-p-phenylenediamine can be formed by heating diphenylamine.

Aniline Compounds↗
PubMed1980

Emulsifiers that enhance susceptibility to virus infection: increased virus penetration and reduced interferon response.

An emulsifier which had an environmental relationship to Reye's syndrome, when used to treated L-929 cultures, was shown to increase the rate of encephalomyocarditis virus penetration and uncoating while having no effect on the attachment of virus or on the replication of infectious ribonucleic acid. This treatment also rendered L-929 cells unable to respond normally to interferon inducers and reversed an already established interferon antiviral state. It is proposed that one or more of these actions result in the cellular enhancement of virus susceptibility.

Animals↗
PubMed1978

Enhanced virus replication in mammalian cells exposed to commercial emulsifiers.

Mammalian cell cultures were used to show that a variety of commercial emulsifiers are capable of enhancing the sensitivity of these cells to infection with several viruses. Some emulsifiers were not active as enhancers, and those viruses that responded to the enhancing emulsifiers were single-stranded ribonucldic acid viruses. The double-stranded viruses that were tested were nonresponders.

Cell Line↗
PubMed1978

Susceptibility of human embryonic kidneys in organ culture to herpesvirus hominis.

101 pairs of human embryonic kidneys of 5-12 weeks' gestation were maintained in whole organ culture by our previously described technique, with herpesvirus hominis types1 and 2 added to our regular media. One kidney of each pair served as a control and was exposed to identical culture medium without virus. Cultures were maintained for 24-120 h to study the time sequence of viral infectivity. Organs were then examined for the presence of virus by electron microscopy and histochemical staining. Histological studies of virus-infected kidneys showed either (1) complete organ death or (2) virus localization in undifferentiated cells, plus disorganization of architecture in differentiated areas. Control organs showed normal organization.

Culture Media↗
PubMed1977

Acute fenitrothion poisoning.

A technician was accidentally exposed to the organophosphorus insecticide fenitrothion and subsequently treated with pralidoxime for the autonomic, somatic and psychiatric manifestations of intoxication. Although long-term therapy with pralidoxime is not recommended, this patient required and obtained symptomatic benefit from its prolonged use. Erythrocytic and plasma cholinesterase activities had been monitored prior to exposure and were monitored throughout treatment and following recovery. Continual monitoring of cholinesterase activities of individuals occupationally exposed to organophosphorus ester insecticides and early diagnosis are essential.

Adult↗