MODELING EXCHANGE RATE VOLATILITIES IN CROATIA

Modeling and forecasting exchange rate volatility has important implications in a range of areas in macroeconomics and finance. A number of models have been developed in empirical finance literature to investigate this volatility across different regions and countries. Well known and frequently applied models to estimate exchange rate volatility are the autoregressive conditional heteroscedastic (ARCH) model advanced by Engle (1982) and the generalized (GARCH) model developed independently by Bollerslev (1986) and Taylor (1986). This paper examines the performance of several ARCH models for the EUR and USD against the HRK on daily data sets within the time period from 1997 to 2015. Evaluating the models through standard information criteria showed that the GARCH (2,1) is the best fitted model  for the EUR/HRK and the GARCH (1,1) for the USD/HRK daily return volatility. In accordance to the estimated models there is no empirical evidence that negative and positive shocks imply a different next period volatility of the daily EUR/HRK as well as the USD/HRK exchange rate return.</p

Immunofluorescence of AQP4 protein expression in each ICH AQP4^+/+ group.

<p>(A) Group of sham operation. (B–D) Groups of ICH 1 d, 3 d, and 7 d. (E–G) Groups of ICH plus VEGF 1 d, 3 d, and 7 d after injection. (H–J) High magnification for groups of sham operation, ICH and ICH plus VEGF 3 d after injection. Arrows show AQP4 labeling is concentrated in glial end-feet surrounding intracerebral capillaries. Scale bar: A–G: 100 µm; H–J: 50 µm.</p

Nissl’s staining of AQP4^+/+ and AQP4^−/− mice.

<p>Injection of rhVEGF165 intracerebroventricularly had no effect on Nissl’s staining in normal mice. At the three time points, marked neuron loss perihemotoma were found in AQP4^−/− mice when compared to AQP4^+/+ mice. Besides, rhVEGF165 increased perihemotomal Nissl’s staining cells in both AQP4^+/+ and AQP4^−/− mice. (A) Groups of control, control plus VEGF and sham operation at 3 d. (B) Groups of ICH and ICH plus VEGF at 1 d, 3 d and 7 d. Astericks represent the hemotoma zones. Scale bar: 50 µm.</p

Western blot of phosphorylation of MAPKs and Akt influenced by rhVEGF165.

<p>RhVEGF165 up-regulated p-JNK and p-ERK at 12 h after administration and expression of the two proteins reached maximum at 48 h (n = 6, *<i>p</i><0.05 vs. 0 h). While no up-regulation of p-p38 or p-Akt was observed within 72 h after rhVEGF165 administration. Besides, expression of AQP4 protein was increased by rhVEGF165 after 24 h and peaked at 48 h (n = 6, *<i>p</i><0.05 vs. 0 h). (A) Western blot image. (B) Semi-quantification analysis.</p

Immunofluorescence of AQP4 protein expression in each normal AQP4^+/+ group.

<p>(A) Negative control without primary antibody gave negative result with no detectable AQP4 labeling. (B, C) High magnification for groups of control and VEGF 3 d after injection showed AQP4 labeling was concentrated in glial end-feet surrounding intracerebral capillaries (arrows). (D–G) Groups of control, VEGF 1 d, 3 d, and 7 d after injection. Vermiform AQP4 with green fluorescence was abundantly expressed after rhVEGF165 injection. Immunofluorescence revealed similar results as Western blot analysis. Scale bar: A, D–G: 100 µm; B, C: 50 µm.</p

Brain water content, brain specific gravity and EB extravasation amount of AQP4^+/+ and AQP4^−/− mice.

<p>(A) Brain tissue water content surrounding the hemotoma in AQP4^+/+ mice was markedly reduced by rhVEGF165 at 1 d, 3 d, and 7 d after intracerebroventricular injection (n = 6, *<i>p</i><0.05 vs. sham operation; & <i>p</i><0.05 vs. ICH), but no effect was observed in AQP4^−/− mice. AQP4^−/− mice had more perihemotomal brain tissue water content than AQP4^+/+ mice in both ICH and ICH plus VEGF groups (n = 6, #<i>p</i><0.05). (B) The specific gravity of brain tissue surrounding hematoma from AQP4^+/+ mice was significantly decreased by rhVEGF165 at 1 d, 3 d, and 7 d after injected intracerebroventricularly (n = 6, *<i>p</i><0.05 vs. sham operation; & <i>p</i><0.05 vs. ICH), while no influence was detected in AQP4^−/− mice. In addition, AQP4^+/+ mice had more specific gravity of perihemotomal brain tissues than AQP4^−/− mice in both ICH and ICH plus VEGF groups (n = 6, #<i>p</i><0.05). Put together, results of the two sections were consistent with each other. (C) In normal mice, the amount of EB extravasation was increased 1 d after intracerebroventricular rhVEGF165 injection in both types of mice, but this effect was only detected in AQP4^−/− mice at 3 d (n = 6, *<i>p</i><0.05 vs. control). No change was found at 7 d. RhVEGF165 had no effect on EB extravasation resulting from ICH whether 1 d, 3 d, or 7 d after intracerebroventricular injection in AQP4^+/+ mice, while an increasing effect in AQP4^−/− mice was found at all time points observed (n = 6, $ <i>p</i><0.05 vs. sham operation; & <i>p</i><0.05 vs. ICH). Meanwhile, this section also showed that AQP4^−/− mice had more EB extravasation than AQP4^+/+ mice in VEGF 1 d, 3 d, all time points of ICH and ICH plus VEGF groups (n = 6, #<i>p</i><0.05).</p

Western blot analysis of AQP4 protein expression in each normal AQP4^+/+ group.

<p>(A, B) Western blot analysis showed rhVEGF165 injected intracerebroventricularly up-regulated AQP4 protein expression at striatum in normal AQP4^+/+ mice at 1 d, 3 d, and 7 d (n = 6, *<i>p</i><0.05 vs. control). (C, D) Western blot analysis showed rhVEGF165 up-regulated perihemotomal AQP4 protein expression at 1 d, 3 d, and 7 d after intracerebroventricular injection (n = 6, *<i>p</i><0.05 vs. sham operation, #<i>p</i><0.05 vs. ICH).</p

AQP4 protein expression in each astrocyte group.

<p>(A) The Western blot image of AQP4 protein. (B) Semi-quantification showed that rhVEGF165 increased AQP4 protein expression in astrocytes, which was inhibited by SP600125 and U0126, but not SB239063 or Ly294002 (n = 6, *<i>p</i><0.05 vs. control, #<i>p</i><0.05 vs. VEGF). (C) Negative control gave negative result without detectable AQP4 labeling. (D) Group of control. (E) Group of VEGF. (F) Group of VEGF plus SP600125. (G) Group of VEGF plus U0126. (H) Group of VEGF plus SB239063. (I) Group of VEGF plus Ly294002. Nuclei are highlighted by DAPI staining. Scale bar: 50 µm.</p

Additional file 3: Figure S3. of The glucagon-like peptide-1 receptor agonist exendin-4 ameliorates warfarin-associated hemorrhagic transformation after cerebral ischemia

Representative immunofluorescence images showed co-localization of Iba1 (green) and TNF-α (red) in microglia. Immunostaining of Iba1(green), TNF-α(red), and DAPI (blue) was performed in the cortical and subcortical areas supplied by the middle cerebral artery. (A) Representative immunofluorescence images showed the percentage of Iba1+/TNF-α + cells to total Iba1+ cells was increased after warfarin treatment. EX-4 treatment reduced the Iba1+/TNF-α + cells percentage, whereas wortmannin blocked this effect of EX-4. Scale bar 50 μm. (B) Quantitative analysis of Iba1 and TNF-α double positive cells/Iba1-positive cells

Additional file 1: Figure S1. of The glucagon-like peptide-1 receptor agonist exendin-4 ameliorates warfarin-associated hemorrhagic transformation after cerebral ischemia

The PT-INR values after warfarin withdrawal. After warfarin withdrawal, INR values remained stable for the next 6 h and dropped to normal values after 24 h. Data are shown as mean ± SD