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Interferon research abs 1 || Hemoglobin research abs || Stem cell research abs || Nucleic acid research abs || Herpes research abs || Bronchitis research abs || Schizophrenia research abs || Tuberculosis research abs || Pneumonia research abs || Constipation research abs || Laxative research abs || hair research abs || hair related research references || testosterone related research references || melanin related research references || caffeine related research references || nicotine related research references







Int J Dev Neurosci. 2000 Dec;18(8):773-780.
Chronic depolarization induced by veratridine increases the survival of rat retinal ganglion cells 'in vitro'

Fernandes Pereira SP, Giestal de Araujo E.

Departamento de Neurobiologia, Instituto de Biologia, Universidade Federal Fluminense, Caixa Postal 100180, 24001-970, Niteroi, RJ, Brazil

During the last decades it has been shown that trophic molecules released by target, afferent and glial cells play a pivotal role controlling neuronal cell death. Trophic molecules are able to inhibit this regressive event during development as well as during degenerative diseases. One of the mechanisms involved in the control of neuronal survival by afferent cells requires the release of trophic molecules stimulated by electrical activity. It has been demonstrated that veratridine (a depolarizing agent that keeps the Na(+) channels opened) induces an increase in neuronal survival. In the present work we show that 3 microM veratridine induced a two-fold increase on the survival of retinal ganglion cells after 48 h in culture. The veratridine effect was inhibited by 50 microM amiloride (an inhibitor of Ca(2+) channels), 25 microM benzamil (an inhibitor of Na(+) channels), 30 microM dantrolene and 7.5 microM caffeine (both inhibitors of Ca(2+) release from the endoplasmatic reticulum) and 10 microM BAPTA-AM (an intracellular Ca(2+) chelator). However, 5 microM nifedipine (a selective inhibitor of voltage-dependent L-type Ca(2+) channels) and 100 microM MK 801 (an inhibitor of NMDA receptors) did not block the veratridine effect. On the other hand, treatment with 10 microM genistein (an inhibitor of tyrosine kinase enzymes), 20 microM fluorodeoxyuridine (an inhibitor of cell proliferation) or 10 microM atropine (an antagonist of muscarinic receptors) completely abolished the effect of veratridine. Taken together, our results indicate that veratridine increases the survival of rat retinal ganglion cells through mechanisms involving Na(+) influx, intracellular Ca(2+) release, activation of tyrosine kinase enzymes and cellular proliferation. They also indicate that cholinergic activity plays an important role in the veratridine effect.


online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=11154846&dopt=Abstract [PubMed - as supplied by publisher]



Eur J Pharm Biopharm. 2001 Jan;51(1):17-24.
Calculation of the dimensions of dosage forms with release controlled by diffusion for in vivo use.

Ainaoui A, Siepmann J, Bodmeier R, Vergnaud JM.

Faculty of Sciences, University of Saint-Etienne, Saint-Etienne, France.

Using numerical models and data obtained from in vitro experiments, the dimensions of diffusion controlled release dosage forms to achieve desired in vivo levels are predicted. Monolithic polymer-drug devices are considered, the release of the drug being controlled by transient diffusion with constant diffusivity. The dimensions of the devices are calculated for various shapes (e.g. spheres, parallelepipeds, cylinders), so that 85% of the drug is released within 6 or 24 h, respectively. Caffeine, diltiazem HCl, and theophylline are studied in ethylcellulose (EC), plasticized with dibutyl sebacate (DBS) or acetyltributyl citrate (ATBC), respectively. The dosage forms are to be administered orally once a day. The resulting drug levels in the plasma are calculated using a numerical model that takes into account: the kinetics of drug release and the pharmacokinetic data of these dosage forms and drugs. Plasma levels resulting from immediate release dosage forms are also calculated, serving as reference.


online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=11154899&dopt=Abstract



Gen Physiol Biophys. 2000 Jun;19(2):237-44.
Distribution of the Ca2+-binding S100A1 protein at different sarcomere lengths of slow and fast rat skeletal muscles.

Maco B, Uhrik B, Heizmann CW.

Institute of Molecular Physiology and Genetics, Slovak Academy of Sciences, Bratislava.

The localization of S100A1 in rat soleus (SOL) and extensor digitorum longus (EDL) muscles was studied immunocytochemically at different sarcomere lengths (stretched, relaxed and contracted) at the ultrastructural level. The muscle fibres were contracted by application of 15 mmol/l caffeine. Following aldehyde fixation, dehydration and embedding in Lowicryl HM20 (-35 degrees C) ultrathin sections were incubated with rabbit polyclonal antiserum against S100A1. Goat antirabbit secondary antibodies conjugated with 10 nm gold particles were used to visualize antigen sites. Relative areas of Z-lines, A- and I-bands were estimated from longitudinal sections by the point counting method. The highest densities of the particles were found at the Z-lines. A higher incidence of S100A1 antigen sites in I-bands than in A-bands and a higher density of S100A1 in lateral parts of A-bands (with actin and myosin filaments overlapping) compared with the central area of A-bands are consistent with an interaction of S100A1 with F-actin in skeletal muscles. Antigen sites were also present at M-lines and at distinct locations of the sarcoplasmic reticulum.


online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=11156445&dopt=Abstract








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