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1.
Physiol Res ; 73(1): 9-25, 2024 03 11.
Article En | MEDLINE | ID: mdl-38466001

No information is available about sex-related differences in unloading-induced cardiac atrophy. We aimed to compare the course of unloading-induced cardiac atrophy in intact (without gonadectomy) male and female rats, and in animals after gonadectomy, to obtain insight into the influence of sex hormones on this process. Heterotopic heart transplantation (HT((x)) was used as a model for heart unloading. Cardiac atrophy was assessed as the weight ratio of heterotopically transplanted heart weight (HW) to the native HW on days 7 and 14 after HTx in intact male and female rats. In separate experimental groups, gonadectomy was performed in male and female recipient animals 28 days before HT(x) and the course of cardiac atrophy was again evaluated on days 7 and 14 after HT(x). In intact male rats, HT(x) resulted in significantly greater decreases in whole HW when compared to intact female rats. The dynamics of the left ventricle (LV) and right ventricle (RV) atrophy after HT(x) was quite similar to that of whole hearts. Gonadectomy did not have any significant effect on the decreases in whole HW, LV, and RV weights, with similar results in male and female rats. Our results show that the development of unloading-induced cardiac atrophy is substantially reduced in female rats when compared to male rats. Since gonadectomy did not alter the course of cardiac atrophy after HTx, similarly in both male and female rats, we conclude that sex-linked differences in the development of unloading-induced cardiac atrophy are not caused by the activity of sex hormones.


Heart Transplantation , Heart , Female , Male , Animals , Rats , Heart Transplantation/adverse effects , Heart Transplantation/methods , Heart Ventricles/pathology , Atrophy/pathology , Gonadal Steroid Hormones , Myocardium/pathology
2.
Ceska Gynekol ; 84(6): 418-424, 2019.
Article En | MEDLINE | ID: mdl-31948249

OBJECTIVE: To analyse own set of molar pregnancies and to develop clinically relevant procedures. TYPE OF STUDY: Review article with analysis of own data. SETTINGS: Department of Pathology 3rd Faculty of Medicine, Charles University, Faculty Hospital Královské Vinohrady, Prague; Department of Obstetrics and Gynecology 3rd Faculty of Medicine, Charles University, Faculty Hospital Královské Vinohrady, Prague. INTRODUCTION: The study monitors the decrease of laboratory values of beta-subunit of hCG gonadotropin (beta-hCG) after evacuation of partial and complete hydatidiform moles in a set of 45 partial and 46 complete moles. Two case reports of invasive moles. RESULTS: In cases of partial hydatidiform moles there was complete regression of beta-hCG in all cases, 89% regressed in six weeks, none of the women showed no subsequent elevation after reaching negativity. In cases of complete hydatidiform moles the decrease was less gradual, the negativity after six weeks was confirmed in 78%, three complete moles became malignant. CONCLUSION: The decrease of beta-hCG after molar pregnancy termination is variable. Even if in cases of complete hydatidiform moles the risk of malignization after reaching negativity is low, beta-hCG checks are recommended at monthly intervals for 6 months. Correct diagnosis of complete mole and its differentiation from partial mole can be achieved using immunohistochemistry - p57 antibody.


Abortion, Induced , Chorionic Gonadotropin, beta Subunit, Human/blood , Hydatidiform Mole, Invasive/pathology , Uterine Neoplasms/pathology , Female , Humans , Hydatidiform Mole, Invasive/blood , Hydatidiform Mole, Invasive/surgery , Immunohistochemistry , Pregnancy , Uterine Neoplasms/blood , Uterine Neoplasms/surgery
3.
Perspect Psychol Sci ; 12(3): 527-542, 2017 05.
Article En | MEDLINE | ID: mdl-28475467

In an anonymous 4-person economic game, participants contributed more money to a common project (i.e., cooperated) when required to decide quickly than when forced to delay their decision (Rand, Greene & Nowak, 2012), a pattern consistent with the social heuristics hypothesis proposed by Rand and colleagues. The results of studies using time pressure have been mixed, with some replication attempts observing similar patterns (e.g., Rand et al., 2014) and others observing null effects (e.g., Tinghög et al., 2013; Verkoeijen & Bouwmeester, 2014). This Registered Replication Report (RRR) assessed the size and variability of the effect of time pressure on cooperative decisions by combining 21 separate, preregistered replications of the critical conditions from Study 7 of the original article (Rand et al., 2012). The primary planned analysis used data from all participants who were randomly assigned to conditions and who met the protocol inclusion criteria (an intent-to-treat approach that included the 65.9% of participants in the time-pressure condition and 7.5% in the forced-delay condition who did not adhere to the time constraints), and we observed a difference in contributions of -0.37 percentage points compared with an 8.6 percentage point difference calculated from the original data. Analyzing the data as the original article did, including data only for participants who complied with the time constraints, the RRR observed a 10.37 percentage point difference in contributions compared with a 15.31 percentage point difference in the original study. In combination, the results of the intent-to-treat analysis and the compliant-only analysis are consistent with the presence of selection biases and the absence of a causal effect of time pressure on cooperation.


Cooperative Behavior , Heuristics , Interpersonal Relations , Decision Making , Humans , Intention , Models, Psychological
4.
Physiol Res ; 64(1): 25-38, 2015.
Article En | MEDLINE | ID: mdl-25194138

The present study was performed to evaluate the role of intrapulmonary activity of the two axes of the renin-angiotensin system (RAS): vasoconstrictor angiotensin-converting enzyme (ACE)/angiotensin II (ANG II)/ANG II type 1 receptor (AT1) axis, and vasodilator ACE type 2 (ACE2)/angiotensin 1-7 (ANG 1-7)/Mas receptor axis, in the development of hypoxic pulmonary hypertension in Ren-2 transgenic rats (TGR). Transgene-negative Hannover Sprague-Dawley (HanSD) rats served as controls. Both TGR and HanSD rats responded to two weeks´ exposure to hypoxia with a significant increase in mean pulmonary arterial pressure (MPAP), however, the increase was much less pronounced in the former. The attenuation of hypoxic pulmonary hypertension in TGR as compared to HanSD rats was associated with inhibition of ACE gene expression and activity, inhibition of AT1receptor gene expression and suppression of ANG II levels in lung tissue. Simultaneously, there was an increase in lung ACE2 gene expression and activity and, in particular, ANG 1-7 concentrations and Mas receptor gene expression. We propose that a combination of suppression of ACE/ANG II/AT1receptor axis and activation of ACE2/ANG 1-7/Mas receptor axis of the RAS in the lung tissue is the main mechanism explaining attenuation of hypoxic pulmonary hypertension in TGR as compared with HanSD rats.


Angiotensin I/metabolism , Hypertension, Pulmonary/prevention & control , Hypoxia/complications , Lung/enzymology , Peptide Fragments/metabolism , Peptidyl-Dipeptidase A/metabolism , Proto-Oncogene Proteins/metabolism , Receptors, G-Protein-Coupled/metabolism , Renin-Angiotensin System , Renin/metabolism , Angiotensin II/metabolism , Angiotensin-Converting Enzyme 2 , Animals , Arterial Pressure , Disease Models, Animal , Hypertension, Pulmonary/enzymology , Hypertension, Pulmonary/genetics , Hypertension, Pulmonary/physiopathology , Hypoxia/enzymology , Hypoxia/physiopathology , Proto-Oncogene Mas , Rats, Sprague-Dawley , Rats, Transgenic , Receptor, Angiotensin, Type 1/metabolism , Renin/genetics , Signal Transduction , Vasoconstriction , Vasodilation
6.
Physiol Res ; 58 Suppl 2: S69-S78, 2009.
Article En | MEDLINE | ID: mdl-20131938

The rat strain transgenic for the murine Ren-2 renin gene (TGR) is defined as a monogenic model of angiotensin II-dependent hypertension with endogenous activation of the renin-angiotensin system. Homozygous males TGR develop malignant hypertension with a strong salt-sensitive component. These animals show severe hypertension, proteinuria and high mortality. Morphological changes of renal parenchyma correspond to chronic ischemic glomerular changes. Heterozygous TGR develop only mild hypertension and thus provide a more suitable model of hypertension regarding to clinical studies. Within the renal parenchyma, secondary focal segmental glomerulosclerosis (FSGS) predominates. High-salt diet in heterozygous animals induces transition from benign to malignant phase of hypertension. In this case, ischemic glomerular changes are superimposed on preexisting secondary FSGS. In the regression model of hypertension (late-onset treatment) the effect of salt intake is attenuated. In homozygous TGR, early selective ET(A) receptor blockade decreased blood pressure and ameliorated end-organ damage. Late selective ET(A) receptor blockade reduced podocyte injury despite final severe hypertension. Survival rate was markedly improved in both regimens with ET(A) selective blockade, while there was only partial improvement with early non-selective blockade. Both bosentan and atrasentan decreased ET-1 levels in both regimens. In heterozygous TGR, early and late ET(A) treatment substantially while ET(A)/ET(B) treatment partially improved survival rate. Significant effect on BP was found with early and late ET(A) blockade, while ET(A)/ET(B) blockade had no effect. Bosentan and atrasentan similarly decreased ET-1 levels on both regimens. In conclusion, selective ET(A) receptor blockade is superior to nonselective ET(A)/ET(B) receptor blockade in attenuating hypertension and end-organ damage. Its effect is more pronounced when applied early in the life.


Antihypertensive Agents/pharmacology , Endothelin A Receptor Antagonists , Glomerulosclerosis, Focal Segmental/prevention & control , Hypertension/drug therapy , Pyrrolidines/pharmacology , Renin/genetics , Sulfonamides/pharmacology , Animals , Atrasentan , Blood Pressure/drug effects , Bosentan , Disease Models, Animal , Disease Progression , Endothelin B Receptor Antagonists , Endothelin-1/metabolism , Glomerulosclerosis, Focal Segmental/genetics , Glomerulosclerosis, Focal Segmental/metabolism , Glomerulosclerosis, Focal Segmental/physiopathology , Heterozygote , Homozygote , Hypertension/complications , Hypertension/genetics , Hypertension/metabolism , Hypertension/physiopathology , Male , Podocytes/drug effects , Podocytes/metabolism , Podocytes/pathology , Rats , Rats, Transgenic , Receptor, Endothelin A/metabolism , Receptor, Endothelin B/metabolism , Sodium Chloride, Dietary , Time Factors
7.
Cesk Fysiol ; 57(4): 104-9, 2008.
Article Cs | MEDLINE | ID: mdl-19526664

Experimental model of 5/6 nephrectomy or the remnant kidney model represents one of the most used animal models of progressive renal failure by reduced nephron number, best-characterized in rats. The reduction of renal mass is achieved by either infarction or surgical excision of both poles, with removal of the contralateral kidney. It enables to investigate the influence of pharmacological, nutritive and other factors on functional and morphological renal parameters. 5/6 nephrectomy produced by infarction is characterised by high plasma renin levels. By contrast, reduction of an equivalent amount of renal parenchyma by surgical excision does not result in the development of hypertension and plasma renin activity is normal to low. The initially normal remnant nephrons undergo compensatory functional and structural adaptations. Simultaneous glomerular hypertension is one of the main factors responsible for the development of renal injury. Morphologicaly progressive focal segmental to global glomerulosclerosis is present, accompanied clinically by increasing proteinuria and deteriorating renal function.


Disease Models, Animal , Kidney Failure, Chronic/physiopathology , Nephrectomy/methods , Nephrons/physiopathology , Adaptation, Physiological , Animals , Disease Progression , Glomerular Filtration Rate , Kidney/pathology , Kidney Failure, Chronic/pathology , Proteinuria , Renal Circulation
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