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T Mainprize

Publications and source records attributed to T Mainprize.

6 recordsLinked to original sources
PubMed1999

June 1999--22 year old female with intraventricular mass.

A 22 year old female presented with a single seizure. CT scan and craniotomy demonstrated an intraventricular papillary tumor with histologic and immunohistochemical features indicative of a choroid plexus carcinoma. Even though the occurrence of this neoplasm is exceptional beyond childhood, pathologists should considered a malignant choroid plexus tumor when postulating the differential diagnosis of intraventricular papillary neoplasms in adults.

Adult↗
PubMed1995

GABA concentrations in the striatum following repetitive cerebral ischemia.

GABAergic neurons in the striatum are very sensitive to the effects of ischemia. The progressive decline in striatal GABA following transient forebrain ischemia in gerbils may be secondary to either a decreased production or an increase in reuptake mechanisms or both. The current experiment was designed to evaluate release of GABA by stimulation with K+ or inhibition of its uptake with nipecotic acid or their combination (K+ nipecotic) after repetitive forebrain ischemia in gerbils by in-vivo microdialysis on Days 1, 3, 5, and 14 following the insult. Infusion of nipecotic acid or potassium chloride, resulted in a significant increase in extracellular GABA. This response was significantly decreased in the post-ischemic animals. The synergistic effect of increased GABA concentrations by the infusion of nipecotic acid + potassium chloride seem in the controls was not evident in the post-ischemic animals. In conclusion, though there is a reduction in the extracellular GABA concentrations in the first week following an ischemic insult, restorative mechanisms are operative in the second week as seen by the increasing GABA concentrations.

Animals↗
PubMed1994

Progressive decrease in extracellular GABA concentrations in the post-ischemic period in the striatum: a microdialysis study.

Repetitive cerebral ischemia in gerbils produces delayed neuronal damage in the substantia nigra reticulata (SNr). This damage begins 4 to 5 days after the insult and is severe by day 7. The damage can be attenuated by GABA agonists. There is a prominent GABAergic striatal pathway to the SNr. Damage to this pathway leads to progressive loss of SNr neurons. This loss can be prevented by GABA agonists. We postulate that, ischemia-induced lack of GABAergic inhibitory input from the striatum to the SNr, may be responsible for this delayed neuronal damage. In the present experiment, we have measured striatal extracellular GABA concentrations with or without nipecotic acid, a GABA-reuptake inhibitor, in gerbils exposed to repetitive ischemia. GABA levels were measured on days 1, 3, 5, and 7 after the ischemic insult. Five control animals and a similar number of ischemic animals were monitored on each day. Extracellular fluid was collected using in vivo microdialysis and GABA levels were measured by electrochemical detection with HPLC. The extracellular striatal GABA levels were very low in the initial three specimens collected, both in the control and in the ischemic animals. However, addition of nipecotic acid resulted in an immediate increase of GABA in measurable range. In comparison to the controls, the increase in GABA on day 1 and 3 were significantly higher in animals with repetitive ischemia (two-way ANOVA with repeated measures). Subsequent measurements showed a gradual decrease in GABA levels when compared to controls. The increase in GABA with nipecotic acid was significantly lower on day 7 after the ischemic insults when compared to the controls. The increased GABA responsiveness immediately after the ischemic insults may reflect a protective effect against excitotoxicity. The subsequent decline in GABA levels after the insult may be secondary to progressive loss of striatal GABAergic neurons. This may contribute to the production of delayed neural damage in the SNr by a decrease in the inhibitory striatal input.

Animals↗
PubMed1990

Characterization of the latency-related transcriptionally active region of the bovine herpesvirus 1 genome.

Approximate 5' and 3' ends of the bovine herpesvirus 1 (BHV-1) latency-related RNA (LR RNA) were mapped in rabbit trigeminal ganglia (TG) by in situ hybridization. The data provide a size estimate of 0.77 to 1.16 kb for the LR RNA. An LR RNA mapping to a similar location was also detected in TG of cattle latently infected with BHV-1. The BHV-1 LR region is transcriptionally active in bovine cell cultures lytically infected with BHV-1. A 1.15-kb transcript, present at early and late times postinfection, of the same sense and approximate size that seen in latently infected TG overlaps a 2.9-kb immediate-early and a 2.6-kb early and late transcription unit present on the complementary strand. Sequence analysis of the LR RNA sense strand indicates the presence of a potential polymerase II promoter in close proximity to the 5' terminus of the LR RNA and two open reading frames within its map positions. The complementary strand contains the 3' portion of a large open reading frame that almost completely overlaps the map position of the LR RNA present on the opposite strand.

Animals↗
PubMed1987

Clinical utility of multiple-dose administration of prostaglandin E2 gel.

An open-label study was undertaken to assess the clinical impact of multiple doses of intracervical prostaglandin E2 (0.5 mg) gel administered at 6-hour intervals. Fifty women with low Bishop scores requiring induction of labor were recruited. The prestudy mean Bishop score was 2.3 +/- 1.1 and changed significantly with one (p less than 0.001), two (p less than 0.001), and three (p less than 0.002) doses. The mean gestational age of patients receiving three doses was significantly less than that of patients receiving one dose, (38.5 versus 40.1 weeks, p less than 0.005). Prostaglandin E2 gel induced labor in 56% of patients, but 14% required subsequent oxytocin (Syntocinon) augmentation. Cesarean section was performed in 6% of patients. No deleterious fetal, neonatal, or maternal effects occurred.

Adult↗