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8 results on '"Kobakhidze, N."'

4. Genetic association study of exfoliation syndrome identifies a protective rare variant at LOXL1 and five new susceptibility loci

Author

Aung, T., Ozaki, M., Lee, M.C., Schlotzer-Schrehardt, U., Thorleifsson, G., Mizoguchi, T., Igo, R.P., Jr., Haripriya, A., Williams, S.E., Astakhov, Y.S., Orr, A.C., Burdon, K.P., Nakano, S., Mori, K., Abu-Amero, K., Hauser, M., Li, Z., Prakadeeswari, G., Bailey, J.N., Cherecheanu, A.P., Kang, J.H., Nelson, S., Hayashi, K., Manabe, S.I., Kazama, S., Zarnowski, T., Inoue, K., Irkec, M., Coca-Prados, M., Sugiyama, K., Jarvela, I., Schlottmann, P., Lerner, S.F., Lamari, H., Nilgun, Y., Bikbov, M., Park, K.H., Cha, S.C., Yamashiro, K., Zenteno, J.C., Jonas, J.B., Kumar, R.S.S., Perera, S.A., Chan, A.S.Y., Kobakhidze, N., George, R., Vijaya, L., Do, T., Edward, D.P., Juan Marcos, L. de, Pakravan, M., Moghimi, S., Ideta, R., Bach-Holm, D., Kappelgaard, P., Wirostko, B., Thomas, S., Gaston, D., Bedard, K., Greer, W.L., Yang, Z, Chen, X., Huang, L., Sang, J., Jia, H., Jia, L., Qiao, C., Zhang, H., Liu, X., Zhao, B., Wang, Y.X., Xu, L., Leruez, S., Reynier, P., Chichua, G., Tabagari, S., Uebe, S., Zenkel, M., Berner, D., Mossbock, G., Weisschuh, N., Hoja, U., Welge-Luessen, U.C., Mardin, C., Founti, P., Chatzikyriakidou, A., Pappas, T., Anastasopoulos, E., Lambropoulos, A., Ghosh, A., Shetty, R., Porporato, N., Saravanan, V., Venkatesh, R., Shivkumar, C., Kalpana, N., Sarangapani, S., Kanavi, M.R., Beni, A.N., Yazdani, S., Hollander, A.I. den, Pasutto, F., Khor, C.C., Aung, T., Ozaki, M., Lee, M.C., Schlotzer-Schrehardt, U., Thorleifsson, G., Mizoguchi, T., Igo, R.P., Jr., Haripriya, A., Williams, S.E., Astakhov, Y.S., Orr, A.C., Burdon, K.P., Nakano, S., Mori, K., Abu-Amero, K., Hauser, M., Li, Z., Prakadeeswari, G., Bailey, J.N., Cherecheanu, A.P., Kang, J.H., Nelson, S., Hayashi, K., Manabe, S.I., Kazama, S., Zarnowski, T., Inoue, K., Irkec, M., Coca-Prados, M., Sugiyama, K., Jarvela, I., Schlottmann, P., Lerner, S.F., Lamari, H., Nilgun, Y., Bikbov, M., Park, K.H., Cha, S.C., Yamashiro, K., Zenteno, J.C., Jonas, J.B., Kumar, R.S.S., Perera, S.A., Chan, A.S.Y., Kobakhidze, N., George, R., Vijaya, L., Do, T., Edward, D.P., Juan Marcos, L. de, Pakravan, M., Moghimi, S., Ideta, R., Bach-Holm, D., Kappelgaard, P., Wirostko, B., Thomas, S., Gaston, D., Bedard, K., Greer, W.L., Yang, Z, Chen, X., Huang, L., Sang, J., Jia, H., Jia, L., Qiao, C., Zhang, H., Liu, X., Zhao, B., Wang, Y.X., Xu, L., Leruez, S., Reynier, P., Chichua, G., Tabagari, S., Uebe, S., Zenkel, M., Berner, D., Mossbock, G., Weisschuh, N., Hoja, U., Welge-Luessen, U.C., Mardin, C., Founti, P., Chatzikyriakidou, A., Pappas, T., Anastasopoulos, E., Lambropoulos, A., Ghosh, A., Shetty, R., Porporato, N., Saravanan, V., Venkatesh, R., Shivkumar, C., Kalpana, N., Sarangapani, S., Kanavi, M.R., Beni, A.N., Yazdani, S., Hollander, A.I. den, Pasutto, F., and Khor, C.C.

Abstract

Item does not contain fulltext, Exfoliation syndrome (XFS) is the most common known risk factor for secondary glaucoma and a major cause of blindness worldwide. Variants in two genes, LOXL1 and CACNA1A, have previously been associated with XFS. To further elucidate the genetic basis of XFS, we collected a global sample of XFS cases to refine the association at LOXL1, which previously showed inconsistent results across populations, and to identify new variants associated with XFS. We identified a rare protective allele at LOXL1 (p.Phe407, odds ratio (OR) = 25, P = 2.9 x 10-14) through deep resequencing of XFS cases and controls from nine countries. A genome-wide association study (GWAS) of XFS cases and controls from 24 countries followed by replication in 18 countries identified seven genome-wide significant loci (P < 5 x 10-8). We identified association signals at 13q12 (POMP), 11q23.3 (TMEM136), 6p21 (AGPAT1), 3p24 (RBMS3) and 5q23 (near SEMA6A). These findings provide biological insights into the pathology of XFS and highlight a potential role for naturally occurring rare LOXL1 variants in disease biology.

Published
2017

6. Dynamics of change of lipid and monoamine metabolisms and the blood coagulation system during experimental atherosclerosis caused by restriction of movement

Author

Gvishiani, G. S and Kobakhidze, N. G

Subjects
Aerospace Medicine
Abstract

Shifts in lipid, catecholamine, and blood coagulation systems following various periods (1, 2, 3, and 4 months) of experimentally induced atherosclerosis were studied. The same indices were studied in the tissues of the myocardium, liver, and brain stem-reticular formation after decapitation of the animals at the end of the experiment. Periodic motion restriction caused an increase in blood beta-lipoproteins in the rabbits at the beginning of the experiment. An increase in general cholesterol content and a decrease in the lecithincholesterol index were established at the end of the experiment. Myocardial beta-lipoprotein and brain stem reticular formation general cholesterol contents were elevated; catecholamine content was increased at the end of the experiment. In the initial months, free adrenaline basically increased, while in later months blood adrenaline decreased and blood noradrenaline increased.

Published
1980

7. Atherosclerotic changes of vessels caused by restriction of movement

Author

Gvishiani, G. S, Kobakhidze, N. G, Mchedlishvili, M. G, and Dekanosidze, T. I

Subjects
Aerospace Medicine
Abstract

The effect of restriction of movement on the development of atheroscelerosis was studied in rabbits. Drastic restriction of movement for 20 and 30 days causes atherosclerotic alterations of the aorta and shifts in ECG which are characteristic of coronary atherosclerosis. At the same time, shortening of the duration of blood coagulation and an increase in the content of catecholamines and beta-lipoproteids occur.

Published
1980

8. [Shifts in the heart left ventricle function in patients with pulmonary tuberculosis during adequate chemotherapy].

Author

Ditiatkov AE, Radzevich AE, Tikhonov VA, and Kobakhidze NI

Subjects
Adult, Aged, Aged, 80 and over, Blood Pressure, Female, Hemodynamics, Humans, Male, Middle Aged, Myocardial Contraction, Tuberculosis, Pulmonary physiopathology, Ventricular Dysfunction, Left physiopathology, Young Adult, Tuberculosis, Pulmonary complications, Tuberculosis, Pulmonary drug therapy, Ventricular Dysfunction, Left drug therapy, Ventricular Dysfunction, Left etiology
Abstract

To investigate the hemodynamics and myocardic contraction of the heart left ventricle, 61 patients with pulmonary tuberculosis (main group) and 26 healthy subjects (control group) were observed. Higher ultimate systolic and diasystolic volumes of the left ventricle and lower levels of the efflux fraction in the patients with active pulmonary tuberculosis were stated. There was shown inverse correlation of the systemic systolic arterial pressure and the left ventricle efflux fraction with ESR, evident of the tuberculosis intoxication. The most pronounced aggravation of the left ventricle function was recorded in the patients with the most severe tuberculosis process. The impairments in the left ventricle in the patients with active pulmonary tuberculosis were of functional nature. Due to intensive therapy of the tuberculosis, the indices of the left ventricle efflux function improved and the systemic arterial pressure came to normal, along with elimination of the tuberculosis intoxication signs.

Published
2010

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