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Biomedical subjects

J H Slott

Publications and source records attributed to J H Slott.

4 recordsLinked to original sources
PubMed1994

Treatment and pathogenesis of traumatic chorioretinal rupture (sclopetaria).

Eight eyes (seven patients) with traumatic chorioretinal rupture (sclopetaria) from severe ocular trauma were examined. All seven patients were referred with diagnoses of retinal detachment, giant retinal tear, or ruptured globe. Instead, all eyes had large, peripheral, full-thickness breaks of the choroid and retina without retinal detachment. Seven of eight eyes were initially managed by observation only; one eye was treated with a scleral buckling procedure. The retina remained attached in all eyes for at least six months. Late retinal detachment (more than one year after initial injury) occurred in two eyes because of retinal breaks at a site distant from the original chorioretinal rupture. Two eyes later developed vitreous hemorrhage associated with posterior vitreous detachment and one of these eyes required vitrectomy to clear the visual axis. The pathogenesis of sclopetaria appears to be mechanical disruption and retraction of tissue rather than acute tissue dissolution. The risk of acute retinal detachment is low. We recommend nonsurgical management for the initial treatment of these patients, with continued observation for complications that may later occur.

Adolescent↗
PubMed1982

Effect of homocysteine and homocystine on platelet and vascular arachidonic acid metabolism.

Normal hemostasis depends in part on the balance achieved between proaggregatory and prothrombotic platelet thromboxane A2, measured as its stable end-product thromboxane B2 (TXB2), and vascular prostacyclin (PGI2), which inhibits platelet aggregation and is antithrombotic. Cystathionine-beta-synthase deficiency is characterized by a high frequency of thromboembolic disease. We therefore studied, in vitro, the effects of homocysteine and related compounds on platelet TXB2 and vascular PGI2 formation. In paired samples of platelet rich plasma, which had been preincubated with L-homocystine (1 mM), mean production of the two platelet cyclooxygenase products, TXB2 and 12-hydroxy-5, 8,10-heptadecatrienoic acid increased significantly from control levels [13.6% +/- 1.9 to 19.8% +/- 2.1 (P less than 0.02) TXB2 and 29.8% +/- 4.2 to 39.4% +/- 4.1 (P less than 0.01) HHT]. In the presence of D,L-homocysteine (1 mM), mean TXB2 and 12-hydroxy-5,8,10-heptadecatrienoic acid production was also significantly increased [12.7% +/- 1.5 to 16.9% +/- 1.5 (P less than 0.01) TXB2 and 27% +/- 4 to 31% +/- 4.1 (P less than 0.02) HHT]. Cystine, cysteine, or methionine (1 mM) did not have similar effects in this test system. Homocysteine and homocystine were without effect on the synthesis of vascular PGI2 by umbilical artery segments [control, 0.22 +/- 0.03 to 0.21 +/- 0.03 ng/mg with D,L-homocysteine and 0.20 +/- 0.04 control to 0.19 +/- 0.04 ng/mg with D,L-homocystine]. A homocyst(e)ine-induced increase in platelet thromboxane production in the absence of an increase in vascular prostacyclin, if present in vivo, may contribute to the vascular thromboses characteristic of human homocystinemias (homocystinurias).

Arachidonic Acid↗
PubMed1981

Decrease prostacyclin production: a characteristic of chronic placental insufficiency syndromes.

Prostacyclin production in neonates born at various gestational ages (28 weeks to term) was compared with that in neonates born of pregnancies complicated by various acute and chronic placental insufficiency states. Prostacyclin levels were reflected by the amount of conversion of 14C arachidonic acid to 6-keto-PGF1 alpha (the stable end-product of prostacyclin) by umbilical arteries. The uptake of 14C arachidonic acid by the umbilical arteries was also determined, and since this was similar for all groups it was not the cause of the differences noted in prostacyclin production. Neonates born of normal pregnancies had similar levels of prostacyclin production regardless of gestational age. Prostacyclin production was very low in neonates born of pregnancies complicated by chronic placental insufficiency (intrauterine growth retardation, essential hypertension, and pre-eclampsia), but normal with acute placental insufficiency (abruptio placentae). Hence the decrease in fetal prostacyclin production in pre-eclampsia is not related to gestational age; furthermore, it is also seen in other chronic placental insufficiency states.

6-Ketoprostaglandin F1 alpha↗