Biomedical subjects

T Vanden Hoek

Publications and source records attributed to T Vanden Hoek.

4 recordsLinked to original sources

PubMed2000

Preconditioning in cardiomyocytes protects by attenuating oxidant stress at reperfusion.

Cardiomyocyte death after ischemia/reperfusion correlates with oxidant stress, and antioxidants confer protection in that model. Preconditioning (PC) with hypoxia or adenosine also confers protection, leading us to hypothesize that PC protects by attenuating oxidant generation during subsequent ischemia/reperfusion. Chick cardiomyocytes were preconditioned with 10 minutes of hypoxia or adenosine (100 micromol/L), followed by 1 hour of simulated ischemia and 3 hours of reperfusion. Adenosine PC decreased cell death from 50+/-3% to 18+/-4% and enhanced the return of contractions during reperfusion, as observed previously with hypoxic PC. A transient burst of dichlorofluorescein (sensitive to H2O2 oxidation that was significantly attenuated by PC initiated by hypoxia or adenosine was seen at reperfusion. The protein kinase C (PKC) inhibitor Go-6976 and the mitochondrial ATP-sensitive K(+) (K(ATP)) channel inhibitor 5-hydroxydecanoate each abolished protection and abrogated the PC-induced attenuation of reperfusion oxidant stress. By contrast, when given only at reperfusion, the K(+) channel opener pinacidil or the antioxidants 2-mercaptopropionylglycine and 1,10-phenanthroline decreased oxidant stress at reperfusion and improved survival and return of contractions. Thus, PC protection is associated with an attenuation of the oxidant burst at reperfusion, regardless of the method by which PC is triggered. Loss of PC protection associated with PKC inhibition or K(ATP) channel inhibitors is associated with a restoration of that oxidant stress. These results suggest a mechanism for PC protection and reveal a functional link between PKC activation and K(ATP) channel activation in that pathway.

Animals↗

PubMed1991

Ultrastructural alterations in the aqueous outflow pathway of adult buphthalmic rabbits.

The aqueous outflow pathway of adult rabbit eyes with congenital glaucoma (buphthalmos) was examined by light microscopy and by scanning and transmission electron microscopy. The morphology of the buphthalmic rabbit aqueous outflow pathway was markedly abnormal when examined at 6 months, 1 yr, and 2 yr displaying apparent loss and/or compression of the iris pillars, dilation of the intertrabecular spaces, loss of endothelial cell-to-cell association and disorganization of trabecular lamellae, and posterior displacement of the aqueous plexus. In addition, the trabecular meshwork lamellae were observed only adjacent to the sclera and the inner portion of the trabecular meshwork was limited to swirls of collagen with scattered cells. These morphological findings suggest that the disease process in the rabbit principally involves an alteration in the differentiation and maintenance of the structural integrity of the trabecular meshwork. The loss of structural support of the buphthalmic trabecular meshwork may be a factor in the wide variation in intraocular pressure and may allow for compression of the trabecular meshwork against the aqueous plexus.

Animals↗

PubMed1990

Cervicothoracic junction injury.

Much emphasis has been placed on evaluating the entire cervical spine through the seventh cervical vertebra. A case of a missed C7-T1 fracture-subluxation with resultant morbidity is presented. A review of the literature reveals the necessity to view the C7-T1 interspace when evaluating cervical spine radiographs. Recommendations are made suggesting closer scrutiny of this region of the spine.

Adult↗

PubMed1987

Vitamin A-induced suppression/enhancement of protein glycosylation and neurulation.

Glycoconjugates play major roles in many cellular functions, e.g. cell migration and cell-to-cell adherence, which are involved in neurulation. The maternal administration of vitamin A on gestation day 8.5 and 9.0 resulted in a high percentage of primary and secondary neurulation defects in gestation day 12 mouse embryos. The neuroepithelium of normal and abnormal embryos was analyzed by one- and two-dimensional sodium dodecyl sulfate polyacrylamide gel electrophoresis and one-dimensional Western blots using concanavalin A (Con A) and peroxidase-conjugated wheat germ agglutinin (WGA) lectins. In vitamin A abnormal embryos, WGA binding was decreased to glycoproteins with apparent molecular weights of 15,000 and 30,000 daltons on Western blots, whereas in vitamin A normal embryos, WGA binding was increased to these glycoproteins on Western blots. Computer-aided fluorescence microscopy using fluorescein isothiocyanate (FITC)-conjugated lectins on 1-micron araldite plastic sections indicated a decrease in FITC-WGA binding to the free surface of nonneurulated neuroepithelium. These results suggest: (1) vitamin A administration may have induced a suppression of WGA-binding carbohydrate residues on 15,000- and 30,000-dalton glycoproteins in abnormal embryos, and (2) modification in the type, amount, and distribution of glycoconjugates may provide a basis for the cellular mechanisms of abnormal development of the neural tube.

Animals↗