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32672. Renaissance and renascences in Western art /
- Creator:
- Panofsky, Erwin,
- Type:
- text and monografie
- Subject:
- Umění, dějiny umění, umění renesanční, novorenesance, historismus, přehledná zpracování světových dějin (chronologicky), and dějiny umění, mecenát
- Language:
- English
- Rights:
- unknown
32673. Renaissance Gothic :
- Creator:
- Kavaler, Ethan Matt
- Type:
- text and monografie
- Subject:
- Architektura, dějiny architektury, architektura gotická, architektura renesanční, světové dějiny středověku (do r. 1492), světové dějiny 1492-1648, and architektura, architekti
- Language:
- English
- Rights:
- unknown
32674. Renaissance Prague /
- Creator:
- Fučíková, Eliška,
- Type:
- text, statický obraz, průvodce, and publikace obrazové
- Subject:
- Výtvarné umění, architektura městská, architektura renesanční, české země 1526-1620, architektura, architekti, and města, obce
- Language:
- English
- Description:
- Přeloženo z češtiny
- Rights:
- unknown
32675. Renaissance thought and Its sources /
- Creator:
- Kristeller, Paul Oskar,
- Type:
- text and monografie
- Subject:
- Dějiny civilizace. Kulturní dějiny, renesance, literatura filozofická, humanismus, písemnictví, literatura, spisovatelé, světové dějiny středověku (do r. 1492), and světové dějiny 1492-1648
- Language:
- English
- Rights:
- unknown
32676. Renaissance: studie o umění výtvarném a poesii
- Creator:
- Pater, Walter and Reichmann, Jan
- Publisher:
- Spolek výtvarných umělců Mánes
- Format:
- print and 151 s.
- Type:
- model:monograph and TEXT
- Subject:
- Umění, estetika, literární kritika, poezie, renesance, umělecká kritika, výtvarné umění, 82-95(049.32), 82-4, 7.072.3(049.32), 21, and 7.01/.09
- Language:
- Czech, English, and French
- Description:
- Walter Pater ; z angličtiny přeložil Jan Reichmann. and Desky nejsou k dispozici.
- Rights:
- http://creativecommons.org/publicdomain/mark/1.0/ and policy:public
32677. Renal activity of Akt kinase in experimental type 1 diabetes
- Creator:
- Jana Ždychová, Jana Veselá, Ludmila Kazdová, and Radko Komers
- Format:
- print, bez média, and svazek
- Type:
- article, články, model:article, and TEXT
- Subject:
- Fyziologie člověka a srovnávací fyziologie, diabetologie, kinázy, diabetická nefropatie, inzulín, diabetology, kinases, diabetic nephropathy, insulin, Akt kinase, mammalian target of rapamycin (mTOR), 14, and 612
- Language:
- English
- Description:
- Akt kinase regulates numerous cell functions including glucose metabolism, cell growth, survival, protein synthesis, and control of local hemodynamics. mTOR is one of down-stream effectors of Akt involved in the initiation of protein translation. However, renal Akt signaling in Type 1 diabetes (DM) in vivo, in particular under the conditions reflecting differences in metabolic control, has received less attention. Renal cortical activity and expression of Akt and mTOR (kinase assay, western blotting) were determined in streptozotocin-diabetic rats (D) with different levels of glycemic control (blood glucose 22.0± 1.0, 13.4±1.5, 8.1±0.4 mmol/l, p<0.05 between the groups), achieved by varying insulin treatment (0,4 and 12 IU/day), and in control rats with (C4) or without (C) chronic insulin administration. Renal Akt activity was reduced in D rats without insulin treatment and severe hyperglycemia (D-0, -62 %, p<0.01 vs. C), partially restored in moderately hypergly cemic rats (D-4, -30 %, p<0.05 vs. C), and normalized in D rats with intensive insulin and tight metabolic control (D-12). Expression of active mTOR paralleled Akt activity in D-0 (-51 %, p<0.01 vs. C), but not in D-4 and D- 12 that demonstrated increases in active mTOR (+55 %, +80 % resp., p<0.05) as compared to C. Moreover, insulin activated renal Akt (+82 %, p<0.01), but not mTOR in C4. In conclusion, glycemic control and intensity of insulin treatment are important modulators of renal Akt and mTOR activity in diabetes. While Akt activity is reversible by tight metabolic control, combination of hyperglycemia and insulin treatment resulted in enhancement of mTOR activity. In addition to Akt, other signaling pathways likely contribute to regulation of renal mTOR activity in diabetes., J. Ždychová, J. Veselá, L. Kazdová, R. Komers., and Obsahuje bibliografii a bibliografické odkazy
- Rights:
- http://creativecommons.org/licenses/by-nc-sa/4.0/ and policy:public
32678. Renal adrenomedullin and high altitude diuresis
- Creator:
- Haditsch, B., Roessler, A., and Helmut Hinghofer-Szalkay
- Format:
- print, bez média, and svazek
- Type:
- article, články, model:article, and TEXT
- Subject:
- Fyziologie člověka a srovnávací fyziologie, fyziologie, nefrologie, adaptace (biologie), physiology, nephrology, adaptation (biology), adrenomedullin, high altitude, hypoxic diuretic response, volume regulation, 14, and 612
- Language:
- English
- Description:
- Previous investigations revealed that most of the fluid regulating hormones showed no consistent relationship to the hypoxic diuretic response (HDR). In this study we examined if adrenomedullin (AM), a hypoxia-mediated diuretic/natriuretic peptide is connected to HDR. Thirty-three persons were examined at low altitude (LA), on the third exposure day at 3440 m (medium altitude, MA) and on the fourteenth day at 5050 m (high altitude, HA). Nocturnal diuresis rose from 460 ml [interquartile range 302 ml] at LA to 560 [660] ml at MA to 1015 [750] ml at HA (p<0.005). Sodium excretion was similar at LA and MA (41.8 [27.0] vs. 41.4 [28.4] mM) and increased to 80.2 [29.1] mM at HA (p<0.005). Urinary AM excretion was 7.9 [3.9] at LA, 7.5 [5.7] pM at MA, and increased to 10.5 [5.1] pM (p<0.05) at HA. Urinary AM excretion was correlated to diuresis (r=0.72, p<0.005) and sodium excretion (r=0.57, p<0.005). Plasma AM concentration rose from 16.4 [3.1] to 18.8 [4.9] pM/l at MA (p<0.005) and to 18.3 [4.3] pM/l at HA (p<0.005). Plasma AM concentration and urinary AM excretion were not correlated, neither were plasma AM concentration and diuresis or natriuresis. Our data suggest the involvement of increased renal AM production in the pathophysiology of high altitude fluid and sodium loss., B. Haditsch, A. Roessler, H. G. Hinghofer-Szalkay., and Obsahuje bibliografii a bibliografické odkazy
- Rights:
- http://creativecommons.org/licenses/by-nc-sa/4.0/ and policy:public
32679. Renal changes in the early stages of diet-induced obesity in ovariectomized rats
- Creator:
- Amaral, L. S. B., Silva, J. A., Trindade, T. M., Ribas, W. B. D., Macedo, C. L., Coimbra, T. M., Belo, N. O., Magalhães, A. C. M., and Soares, T. J.
- Format:
- print, bez média, and svazek
- Type:
- article, články, model:article, and TEXT
- Subject:
- Fyziologie člověka a srovnávací fyziologie, ledviny, obezita, dietní jídla, kidneys, obesity, diet, ovariectomy, renal inflammation, 14, and 612
- Language:
- English
- Description:
- The relationship between obesity and renal lesions, especially in low estrogen levels, has been less documented. The aim of this study was to assess the renal changes in diet-induced obesity in ovariectomized rats. Wistar rats were ovariectomized or shamoperated and divided into four groups: sham-operated rats fed a standard diet (SSD); ovariectomized rats fed a standard diet (OSD); sham-operated rats fed a high-fat diet (SHFD); ovariectomized rats fed a high-fat diet (OHFD). Body weight and blood pressure were measured weekly. The rats were killed 24 weeks after initiation of standard or high-fat diet treatment, the kidneys were removed for immunohistochemical and histological studies. Blood and urine samples were collected to quantify sodium, potassium and creatinine. OHFD rats presented increases in visceral adipose tissue, serum insulin levels, blood pressure and proteinuria, and a decrease in fractional excretion of sodium as well. Histological and morphometric studies showed focal alterations in the renal cortex. Expression of macrophages, lymphocytes, nuclear factor-kappa B (NF-B), Proliferating Cell Nuclear Antigen (PCNA), angiotensin II (ANG II) and vimentin was greater in OHFD rats than in control rats. Thus, these results demonstrate that the high-fat diet in ovariectomized rats promoted renal function and structure changes, renal interstitial infiltration of mononuclear cells and increased expression of ANG II and NF-κB., L. S: B. Amaral, J. A. Silva, T. M. Trindade, W. B. D. Ribas, C. L. Macedo, T. M. Coimbra, N. O. Belo, A. C. M. Magalhães, T. J. Soares., and Obsahuje bibliografii
- Rights:
- http://creativecommons.org/licenses/by-nc-sa/4.0/ and policy:public
32680. Renal Concentrating Capacity is Linked to Blood Pressure in Children with Autosomal Dominant Polycystic Kidney Disease
- Creator:
- Seeman, T., Dušek, J., Vondrák, K., Bláhová, K., Šimková, E., Kreisinger, J., Dvořák, P., Kynčl, M., Hříbal , Z., and Janda, J.
- Type:
- article, model:article, and TEXT
- Subject:
- Renal concentrating capacity test, Autosomal dominant polycystic kidney disease, Blood pressure, Hypertension, and Children
- Language:
- English
- Description:
- Impaired glomerular filtration rate (GFR) is a risk factor for the development of hypertension in patients with autosomal dominant polycystic kidney disease (ADPKD). However, markers of tubular function were not tested whether they are linked to hypertension or blood pressure (BP) level. The aim of our study was to investigate the relationship between renal concentrating capacity and BP in children with ADPKD. Fifty-three children (mean age 11.84.4 years) were investigated. Standardized renal concentrating capacity test was performed after nasal drop application of desmopressin, BP was measured by ambulatory BP monitoring (ABPM). Renal concentrating capacity was decreased in 58 % of children. The prevalence of hypertension was significantly higher in children with decreased renal concentrating capacity (35 %) than in children with normal renal concentrating capacity (5 %) (p0.05). Significant negative correlations were found between renal concentrating capacity, ambulatory BP and number of renal cysts (r = –0.29 to –0.39, p0.05 to p0.01). In conclusion, the concentrating capacity is decreased in about half of the patients and is linked to BP. Decreased renal concentrating capacity should be considered as an early marker of functional impairment in ADPKD and a further risk factor for hypertension.
- Rights:
- http://creativecommons.org/licenses/by-nc-sa/4.0/ and policy:public