Juan Arango | Universidad Central de Venezuela (original) (raw)

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Papers by Juan Arango

Research paper thumbnail of Exponentially convex univalent functions

Research paper thumbnail of Comparison of N-acetylglucosaminyltransferase V activities in Rous sarcoma-transformed baby hamster kidney (RS-BHK) and BHK cells

Journal of Cellular Biochemistry, 1988

Recent studies have desmonstrated that Rous sarcoma virus-transformed baby hamster kidney (RS-BHK... more Recent studies have desmonstrated that Rous sarcoma virus-transformed baby hamster kidney (RS-BHK) cells express twofold higher levels of those N-linked oligosac-charides that contain the sequence [GlcNAc-β(1,6)Man (1,6)] compared to nontrans-formed parental BHK cells (Pierce and Arango, J. Biol. Chem. 261, 10772 [1986]). We have investigated in RS-BHK and BHK cells the activity of UDP-GlcNAc:α-D-mannoside β(l,6)N-acetylglucosaminyltransferase V, the enzyme that begins the synthesis of the sequence that is increased in the RS-BHK cells. We have measured GnT V activity using UDP- [3H]- GlcNAc and a synthetic oligosaccharide acceptor, GlcNAcβ(1,2)Man α(1,6)Manβ-O- (Ch2)8COOCH3, separating the radioactive product by a newly devised reverse-phase chromatographic technique. Assayed under optimal conditions, the specific activity of GnT V is about fourfold higher in RS-BHK sonicates than in BHK sonicates, suggesting that this increase in activity may be the primary mechanism that causes the increase in [GlcNAcβ(1,6) Man] sequences in the RS-BHK cells. The apparent Km, values of the enzymes in RS-BHK and BHK cell sonicates for UDP-GIcNAc and the synthetic acceptor are similar, as are the pH optima. These results suggest that the increase in GnT V-specific activity in RS-BHK cells is not caused by the presence in these cells of a GnT V with markedly different kinetic properties.

Research paper thumbnail of The impact of different presenilin 1 andpresenilin 2 mutations on amyloid deposition, neurofibrillary changes and neuronal loss in the familial Alzheimer's disease brain: Evidence for other phenotype-modifying factors

Brain, 1999

To assess the influence of the presenilin 1 (PS1) and 2 (PS2) mutations on amyloid deposition, ne... more To assess the influence of the presenilin 1 (PS1) and 2 (PS2) mutations on amyloid deposition, neurofibrillary tangle (NFT) formation and neuronal loss, we performed stereologically based counts in a high-order association cortex, the superior temporal sulcus, of 30 familial Alzheimer's disease cases carrying 10 different PS1 and PS2 mutations, 51 sporadic Alzheimer's disease cases and 33 non-demented control subjects. All the PS1 and PS2 mutations assessed in this series led to enhanced deposition of total Aβ and Aβ x-42/43 but not Aβ x-40 senile plaques in the superior temporal sulcus when compared with brains from sporadic Alzheimer's disease patients. Some of the Abbreviations: ANOVA ϭ analysis of variance; APOE ϭ apolipoprotein E; APP ϭ amyloid-β protein precursor; NFT ϭ neurofibrillary tangles; PS1 ϭ presenilin 1; PS2 ϭ presenilin 2 © Oxford University Press 1999 PS1 mutations studied (M139V, I143F, G209V, R269H, E280A), but not others, were also associated with faster rates of NFT formation and accelerated neuronal loss in the majority of the patients who harboured them when compared with sporadic Alzheimer's disease patients. In addition, our analysis showed that dramatic quantitative differences in clinical and neuropathological features can exist even among family members with the identical PS mutation. This suggests that further individual or pedigree genetic or epigenetic factors are likely to modulate PS phenotypes strongly.

Research paper thumbnail of On force and tooth movement

American Journal of Orthodontics, 1970

Research paper thumbnail of El origen de la vida

Desde que el hombre tuvo la capacidad de pesar y de razonar, se empezó a preguntar como surgió la... more Desde que el hombre tuvo la capacidad de pesar y de razonar, se empezó a preguntar como surgió la vida, surgiendo así uno de los problemas más complejos y difíciles que se ha planteado el ser humano, en su afán de encontrar una respuesta, se intento solucionarlo mediante explicaciones religiosas, mitológicas y científicas, a partir de estas ultimas han surgido varias teorías y otras han sido descartadas.

Research paper thumbnail of Exponentially convex univalent functions

Research paper thumbnail of Comparison of N-acetylglucosaminyltransferase V activities in Rous sarcoma-transformed baby hamster kidney (RS-BHK) and BHK cells

Journal of Cellular Biochemistry, 1988

Recent studies have desmonstrated that Rous sarcoma virus-transformed baby hamster kidney (RS-BHK... more Recent studies have desmonstrated that Rous sarcoma virus-transformed baby hamster kidney (RS-BHK) cells express twofold higher levels of those N-linked oligosac-charides that contain the sequence [GlcNAc-β(1,6)Man (1,6)] compared to nontrans-formed parental BHK cells (Pierce and Arango, J. Biol. Chem. 261, 10772 [1986]). We have investigated in RS-BHK and BHK cells the activity of UDP-GlcNAc:α-D-mannoside β(l,6)N-acetylglucosaminyltransferase V, the enzyme that begins the synthesis of the sequence that is increased in the RS-BHK cells. We have measured GnT V activity using UDP- [3H]- GlcNAc and a synthetic oligosaccharide acceptor, GlcNAcβ(1,2)Man α(1,6)Manβ-O- (Ch2)8COOCH3, separating the radioactive product by a newly devised reverse-phase chromatographic technique. Assayed under optimal conditions, the specific activity of GnT V is about fourfold higher in RS-BHK sonicates than in BHK sonicates, suggesting that this increase in activity may be the primary mechanism that causes the increase in [GlcNAcβ(1,6) Man] sequences in the RS-BHK cells. The apparent Km, values of the enzymes in RS-BHK and BHK cell sonicates for UDP-GIcNAc and the synthetic acceptor are similar, as are the pH optima. These results suggest that the increase in GnT V-specific activity in RS-BHK cells is not caused by the presence in these cells of a GnT V with markedly different kinetic properties.

Research paper thumbnail of The impact of different presenilin 1 andpresenilin 2 mutations on amyloid deposition, neurofibrillary changes and neuronal loss in the familial Alzheimer's disease brain: Evidence for other phenotype-modifying factors

Brain, 1999

To assess the influence of the presenilin 1 (PS1) and 2 (PS2) mutations on amyloid deposition, ne... more To assess the influence of the presenilin 1 (PS1) and 2 (PS2) mutations on amyloid deposition, neurofibrillary tangle (NFT) formation and neuronal loss, we performed stereologically based counts in a high-order association cortex, the superior temporal sulcus, of 30 familial Alzheimer's disease cases carrying 10 different PS1 and PS2 mutations, 51 sporadic Alzheimer's disease cases and 33 non-demented control subjects. All the PS1 and PS2 mutations assessed in this series led to enhanced deposition of total Aβ and Aβ x-42/43 but not Aβ x-40 senile plaques in the superior temporal sulcus when compared with brains from sporadic Alzheimer's disease patients. Some of the Abbreviations: ANOVA ϭ analysis of variance; APOE ϭ apolipoprotein E; APP ϭ amyloid-β protein precursor; NFT ϭ neurofibrillary tangles; PS1 ϭ presenilin 1; PS2 ϭ presenilin 2 © Oxford University Press 1999 PS1 mutations studied (M139V, I143F, G209V, R269H, E280A), but not others, were also associated with faster rates of NFT formation and accelerated neuronal loss in the majority of the patients who harboured them when compared with sporadic Alzheimer's disease patients. In addition, our analysis showed that dramatic quantitative differences in clinical and neuropathological features can exist even among family members with the identical PS mutation. This suggests that further individual or pedigree genetic or epigenetic factors are likely to modulate PS phenotypes strongly.

Research paper thumbnail of On force and tooth movement

American Journal of Orthodontics, 1970

Research paper thumbnail of El origen de la vida

Desde que el hombre tuvo la capacidad de pesar y de razonar, se empezó a preguntar como surgió la... more Desde que el hombre tuvo la capacidad de pesar y de razonar, se empezó a preguntar como surgió la vida, surgiendo así uno de los problemas más complejos y difíciles que se ha planteado el ser humano, en su afán de encontrar una respuesta, se intento solucionarlo mediante explicaciones religiosas, mitológicas y científicas, a partir de estas ultimas han surgido varias teorías y otras han sido descartadas.

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