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Biomedical subjects

C T King

Publications and source records attributed to C T King.

7 recordsLinked to original sources
PubMed1992

Fatal disseminated Conidiobolus coronatus infection in a renal transplant patient.

A case of fatal disseminated fungal infection due to Conidiobolus coronatus in a patient with a renal transplant is described. This organism, known to cause localized infections in otherwise healthy individuals in the tropics, is now recognized as a cause of fatal infection in immunosuppressed hosts. Histologically, localized infections are characterized by lack of vessel invasion and the presence of an eosinophilic sleeve around fungal elements, called the Splendore-Hoeppli phenomenon. The histologic findings in the present case were more typical of mucormycosis, and the correct diagnosis was established only after the organism was isolated and identified in culture.

Cytomegalovirus Infections↗
PubMed1991

Dietary sodium chloride deprivation throughout development selectively influences the terminal field organization of gustatory afferent fibers projecting to the rat nucleus of the solitary tract.

In order to determine whether the developing central gustatory system responds to altered sensory experience, terminal fields of the chorda tympani nerve (CT) within the nucleus of the solitary tract (NTS) in control, NaCl deprived, and rats in which CT taste responses "recovered" from NaCl deprivation were investigated via anterograde transport of HRP. Rats fed a low sodium diet (0.03% NaCl) from the third day of gestation to at least 35 days postnatal exhibited both abnormally distributed and irregularly shaped CT terminal fields. Specifically, the dorsal zone of the field was the smallest in controls whereas it was the largest in deprived rats, occupying more medial and caudal territory within the nucleus. The portion of the field immediately ventral to the dorsalmost zone was characterized by a compact, oval shape in control rats and an irregular, broad configuration in deprived rats. Although it has been observed that deprivation-induced changes in the neurophysiology of the CT are reversible, the central morphological alterations reported here remain abnormal. Restoration of 1.0% NaCl in the diet at 28 days postnatally, for at least 60 days, did not result in normal CT terminal fields. The pattern of the field in rats "recovered" from NaCl deprivation was comparable to that found in deprived rats, and the size of the field was three times that found in control and deprived rats. The terminal fields of another nerve containing gustatory afferents, the lingual-tonsilar branch of the glossopharyngeal nerve (LT-IX), were studied for comparison. Interestingly, the pattern of the LT-IX field was not altered by sodium deprivation. The relative size and topography of the LT-IX fields in deprived rats were similar to controls. Thus, sodium deprivation appears to alter selectively the anatomical organization of the CT. Differences in vulnerability between the CT and LT-IX terminal fields may derive from differences in the responsiveness of these nerves to NaCl, and/or to differences in the timing of early neural events.

Afferent Pathways↗
PubMed1978

Enhancement of chlorcyclizine teratogenicity in the rat by coadministration of calcium chelating agents.

Chlorcyclizine and structurally related drugs induce a high incidence of cleft palate and skeletal malformations in fetal rats. We have shown previously that these teratogens bind tightly and reversibly to chondroitin sulfate of cartilage and compete with calcium for binding. Experiments reported here demonstrate that co-administration of calcium chelating agents with chlorcyclizine significantly increases both the frequency of malformations and retention of [14C] chlorcyclizine by embryos. Retention of radioactive teratogen by embryos is inverse to retention of [45Ca]calcium. These findings suggest that drug binding to embryonic glycosaminoglycans is involved in the pathogenesis of malformations produced by chlorcyclizine.

Abnormalities, Drug-Induced↗
PubMed1978

Chlorcyclizine induction of cleft palate in the rat: degradation of palatal glycosaminoglycans.

Administration of the cleft palate teratogen chlorcyclizine or norchlorcyclizine to pregnant rats causes an alteration in glycosaminoglycans (GAGs) in embryonic palatal shelves. Pulse-chase experiments in vitro indicate that norchlorcyclizine enhances the degradation of hyaluronic acid and chondroitin sulfate but has little or no effect on their synthesis. These changes in GAGs are caused by concentrations of norchlorcyclizine that have no appreciable effect on DNA or protein synthesis. These findings suggest that degradation of palatal GAGs may be the primary biochemical defect responsible for the inhibition of palatal shelf elevation by norchlorcyclizine.

Abnormalities, Drug-Induced↗