The International Monetary Fund in the Contemporary World Economy

katedra: KEK; přílohy: 1 CD; rozsah: 69 stran, 4. s. přílohThis dissertation deals with the activities of the International Monetary Fund (IMF) from the time of its establishment, as a reaction to the situation of the world economy after the World War II, to this time, when the IMF has to react on the development of the world financial system. At first, the work introduces some general dates about the IMF, describes the spheres of its activity and shows its reaction to the changes of the financial system. The second part of this work deals with the financial crises, which have impacted some countries and regions. The work investigates the causes of these crises, its continuance and the asset of the IMF to its solutions. The last part plans some possible changes in the activity of the International Monetary Fund, which can help to the better and more stable world financial system.Diplomová práce se zabývá činností Mezinárodního měnového fondu (IMF) od jeho založení, coby reakce na neuspořádaný stav světového hospodářství po druhé světové válce, až do současné doby, kdy Mezinárodní měnový fond musí rychle a pohotově reagovat na vývoj finanční soustavy. Práce nejprve uvádí obecné údaje o IMF, popisuje oblasti jeho působnosti a všímá si jeho reakcí na změny finančního systému. V druhé polovině se zabývá finančními krizemi, které zasáhly některé země i regiony na přelomu tisíciletí. Zkoumá příčiny těchto krizí, jejich průběh a analyzuje přínos Mezinárodního měnového fondu k jejich řešení. Poslední část práce navrhuje možné změny v činnosti Mezinárodního měnového fondu, které by mohly přispět k lepšímu a stabilnějšímu mezinárodnímu finančnímu systému

Non-isotopic detection of nucleolar transcription in pre-implantation mouse embryos

International audienc

Correction: Targeting of the Plzf Gene in the Rat by Transcription Activator-Like Effector Nuclease Results in Caudal Regression Syndrome in Spontaneously Hypertensive Rats.

[This corrects the article DOI: 10.1371/journal.pone.0164206.]

Effects of Metformin on Tissue Oxidative and Dicarbonyl Stress in Transgenic Spontaneously Hypertensive Rats Expressing Human C-Reactive Protein.

Inflammation and oxidative and dicarbonyl stress play important roles in the pathogenesis of type 2 diabetes. Metformin is the first-line drug of choice for the treatment of type 2 diabetes because it effectively suppresses gluconeogenesis in the liver. However, its "pleiotropic" effects remain controversial. In the current study, we tested the effects of metformin on inflammation, oxidative and dicarbonyl stress in an animal model of inflammation and metabolic syndrome, using spontaneously hypertensive rats that transgenically express human C-reactive protein (SHR-CRP). We treated 8-month-old male transgenic SHR-CRP rats with metformin (5 mg/kg/day) mixed as part of a standard diet for 4 weeks. A corresponding untreated control group of male transgenic SHR-CRP rats were fed a standard diet without metformin. In a similar fashion, we studied a group of nontransgenic SHR treated with metformin and an untreated group of nontransgenic SHR controls. In each group, we studied 6 animals. Parameters of glucose and lipid metabolism and oxidative and dicarbonyl stress were measured using standard methods. Gene expression profiles were determined using Affymetrix GeneChip Arrays. Statistical significance was evaluated by two-way ANOVA. In the SHR-CRP transgenic strain, we found that metformin treatment decreased circulating levels of inflammatory response marker IL-6, TNFα and MCP-1 while levels of human CRP remained unchanged. Metformin significantly reduced oxidative stress (levels of conjugated dienes and TBARS) and dicarbonyl stress (levels of methylglyoxal) in left ventricles, but not in kidneys. No significant effects of metformin on oxidative and dicarbonyl stress were observed in SHR controls. In addition, metformin treatment reduced adipose tissue lipolysis associated with human CRP. Possible molecular mechanisms of metformin action-studied by gene expression profiling in the liver-revealed deregulated genes from inflammatory and insulin signaling, AMP-activated protein kinase (AMPK) signaling and gluconeogenesis pathways. It can be concluded that in the presence of high levels of human CRP, metformin protects against inflammation and oxidative and dicarbonyl stress in the heart, but not in the kidney. Accordingly, these cardioprotective effects of metformin might be especially effective in diabetic patients with high levels of CRP

Folate Deficiency Is Associated With Oxidative Stress, Increased Blood Pressure, and Insulin Resistance in Spontaneously Hypertensive Rats

BackgroundThe role of folate deficiency and associated hyperhomocysteinemia in the pathogenesis of metabolic syndrome is not fully established. In the current study, we analyzed the role of folate deficiency in pathogenesis of the metabolic syndrome in the spontaneously hypertensive rat (SHR).MethodsMetabolic and hemodynamic traits were assessed in SHR/Ola rats fed either folate-deficient or control diet for 4 weeks starting at the age of 3 months.ResultsCompared to SHRs fed a folate-replete diet, SHRs fed a folate-deficient diet showed significantly reduced serum folate (104 ± 5 vs. 11 ± 1 nmol/L, P < 0.0005) and urinary folate excretion (4.3 ± 0.6 vs. 1.2 ± 0.1 nmol/16 h, P < 0.0005) together with a near 3-fold increase in plasma total homocysteine concentration (4.5 ± 0.1 vs 13.1 ± 0.7 μmol/L, P < 0.0005), ectopic fat accumulation in liver, and impaired glucose tolerance. Folate deficiency also increased systolic blood pressure by approximately 15 mm Hg (P < 0.01). In addition, the low-folate diet was accompanied by significantly reduced activity of antioxidant enzymes and increased concentrations of lipoperoxidation products in liver, renal cortex, and heart.ConclusionsThese findings demonstrate that the SHR model is susceptible to the adverse metabolic and hemodynamic effects of low dietary intake of folate. The results are consistent with the hypothesis that folate deficiency can promote oxidative stress and multiple features of the metabolic syndrome that are associated with increased risk for diabetes and cardiovascular disease

Caudal regression syndrome in fetuses of <i>Plzf</i> deficient rats.

<p>In comparison to wild-type <b>(A, D)</b>, or heterozygous <b>(H)</b> rat fetuses, note the markedly reduced length and missing (delayed) ossification of the long bones (arrows) in <i>Plzf</i>^<i>-/-</i> rats <b>(B, C, E). (B)</b> Left foot shows normal number of 5 metatarsal bones, but a duplication of the 2^nd finger. In contrast, a toe is absent on the right side of this animal. <b>(C)</b> Bilateral oligodactyly. <b>(E)</b> Absence of the 1^st metatarsal bone and toe, and duplication of the 3^rd finger. <b>(F)</b> Oligodactyly on the left foot after fixation in Bouin-Hollande fluid, which gives the green colour to the specimen. <b>(G)</b> Oligodactyly and thin and bent tail tip. <b>(H)</b> The tail of the <i>Plzf</i> ^<i>+/-</i> rat with strong reduction of the number of tail vertebrae; note the absence of vertebrae in the terminal part of the tail. <b>(I)</b> A thin and bent tail tip in a postnatal <i>Plzf</i>^<i>-/-</i> rat.</p

Derivation of <i>Plzf</i>-null rat.

<p><b>(A)</b> Design of the TAL effector endonuclease to target exon 2 (first coding exon) of <i>Plzf</i> gene. Two key aminoacid residues recognising each base of the target are shown. FokI = FokI endonuclease domain. <b>(B)</b> Screening of pups from microinjected zygotes by Surveyor endonuclease—left panel, second lane (first sample) represents the founder with cleaved heteroduplex (arrowheads). Interestingly, the heteroduplex was visible on native polyacrylamide elecrophoresis gel (without Surveyor treatment)–right panel, arrowhead. <b>(C)</b> Sequencing of the founder´s <i>Plzf</i>–comparison of the mutated and wild-type allele. Note NciI recognition site in the wild-type sequence. <b>(D)</b> Comparison of predicted amino acid sequence of the wild-type and targeted <i>Plzf</i> shows truncation of the protein. <b>(E)</b> Example of genotyping the targeted mutants with PCR followed by restriction digestion by NciI. Mutant allele is not cleaved. <b>(F)</b> Western blotting using N-terminal anti-PLZF antibody in the heart, liver, kidney and skeletal muscle in <i>Plzf</i>^<i>-/-</i> mutant homozygote and wild-type animals.</p