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

α-Synuclein overexpression increases its localization on mitochondria without causing mitochondrial fragmentation in PC12 cells.

<p><b>A.</b> Representative double-staining images of α-synuclein (Green) and mitochondria (Red) in PC12 cells transfected with <i>SNCA</i> or an empty vector for 48 h. Amplified images clearly demonstrate that no perceptible alteration in mitochondrial morphology between these two groups. Cytofluorogram analysis shows that PC coefficient of that α-synuclein overexpressed cell (PC = 0.574982, CC Mx = 0.972038, CC My = 0.98707) is much higher than Vector group (PC = 0.316512, CC Mx = 0.962559, CC My = 0.439231). Scale bars for 10 µm. B. Quantitative analysis shows that PC coefficients in <i>SNCA</i> group are remarkably elevated compared with Vector group. C. Immunoblotting assay shows that α-synuclein expression levels in PC12 cell lysates and mitochondrial lysates are both significantly increased after <i>SNCA</i> transfection for 48 h (n = 4). <b>D.</b> Quantitative analysis of changes in mitochondrial length shows no significant statistic difference between <i>SNCA</i> group and Vector group. Images of 20 cells from each group were processed for cytofluorogram (B) and mitochondrial morphology analysis (D), and the experiment was repeated three times. *P<0.05, **P<0.01.</p

Cell Fixation Does not Alter Mitochondrial Morphology Probed by Staining with MitoTracker-Red CMXRos.

<p><b>A.</b> Representative images of mitochondria in the same SH-SY5Y cells stained with MitoTracker-Red CMXRos were taken immediately before and 30 min after fixation with 4% paraformaldehyde on live cell imaging system. Mitochondrial morphology in SH-SY5Y cells remains almost the same after fixation for 30 min. Scale bars for 10 µm. <b>B.</b> Quantitative analysis of changes in mitochondrial length of the same SH-SY5Y cells in images taken immediately before and 30 min after fixation. The experiment was carried out five times, and no perceptible difference in mitochondrial length is detected in SH-SY5Y cells after fixation.</p

The effects of α-synuclein suppression on mitochondrial morphology in SH-SY5Y cells.

<p>Representative images taken by live cell imaging system show no obvious alteration in mitochondrial morphology between Neg group (A) and RNAi group (D). MPP⁺ (1 mM) induces severe mitochondrial fragmentation in Neg group (B and C) but has little effect on mitochondrial morphology in RNAi group (E and F). Scale bar for 10 µm.</p

α-Synuclein knockdown prevents MPP⁺-induced cell apoptosis and mitochondrial fragmentation in SH-SY5Y cells.

<p><b>A.</b> Immunoblotting assay demonstrates that α-synuclein expression is remarkably suppressed in SH-SY5Y cells transfected with <i>SNCA</i> siRNA (RNAi group) for 2–5 d, yet it is hardly affected in cells transfected with a negative control sequence (Neg group) (n = 5). <b>B.</b> Quantitative analysis of changes in mitochondrial length shows that MPP⁺ (1 mM) decreases mitochondrial length in Neg group, however, it has little effect on the index in RNAi group. Images of 20 cells from each group were processed for mitochondrial morphology analysis, and the experiment was repeated three times. <b>C.</b> Flow cytometric analysis of cell apoptosis shows that MPP⁺ leads to severe cell injury in Neg group, while it slightly harms SH-SY5Y cells in RNAi group (n = 4). *P<0.05, **P<0.01, ***P<0.001 Neg versus RNAi; #P<0.05, ##P<0.01, ###P<0.001 compared with Neg control.</p

α-Synuclein Distribution Patterns and Mitochondrial Morphology in Three Cell Lines.

<p><b>A.</b> Representative double-staining images show the patterns of α-synuclein distribution (green) and mitochondrial morphology (red) in SH-SY5Y, PC12 and Hela cells. Low levels of α-synuclein were expressed in all three cell lines, and it distributes in a small dotted fashion. α-Synuclein is relatively highly expressed in the nucleus in SH-SY5Y and Hela cells other than in PC12 cells. Amplified images further demonstrate that only a small part of cytoplasmic immunofluorescent staining of α-synuclein co-localizes with mitochondria in SH-SY5Y and Hela cells, while most of cytoplasmic α-synuclein reside in mitochondria in PC12 cells. Scale bars for 10 µm. <b>B.</b> Cytofluorogram analysis of the double-staining images above shows that Pearson's Correlation (PC) coefficient is much higher in PC12 cells than those in SH-SY5Y and Hela cells. CC, colocalization coefficient.</p

α-Synuclein overexpression in Hela cells promotes its co-localization with mitochondria without affecting mitochondrial morphology.

<p><b>A.</b> Representative double-staining images of α-synuclein (Green) and mitochondria (Red) in Hela cells transfected with <i>SNCA</i> or an empty vector for 48 h. Further amplified images show that no obvious change in mitochondrial morphology between these two groups. Cytofluorogram analysis demonstrates that PC coefficient in that α-synuclein overexpressed cell is remarkably elevated (PC = 0.374221, CC Mx = 0.998574, CC My = 0.845116) compared with Vector group (PC = −0.0338751, CC Mx = 0.905173, CC My = 0.796768). Scale bars for 10 µm. B. Quantitative analysis demonstrates that PC coefficients in <i>SNCA</i> group are much higher than Vector group. C. Immunoblotting assay demonstrates that α-synuclein expression levels in Hela cell lysates and mitochondrial lysates are both remarkably increased after <i>SNCA</i> transfection for 48 h (n = 4). <b>D.</b> Quantitative analysis of changes in mitochondrial length shows no significant statistic difference between <i>SNCA</i> group and Vector group. Images of 20 cells from each group were processed for cytofluorogram (B) and mitochondrial morphology analysis (D), and the experiment was repeated three times. *P<0.05, **P<0.01.</p

NSP inhibits the release of NO and TNF-α.

<p>The releases of NO (A) and TNF-α (B) from the OGD12h-treated cells after 12- and 24-h of reoxygenation were significantly reduced by NSP administration. The gray columns indicate the control groups (without NSP administration), whereas the white columns indicate the groups treated with 5 ng/mL of NSP. * P < 0.05, NSP group vs. non-NSP group.</p

Effects of NSP and the NF-κB inhibitor, sc3060.

<p>A. The morphological changes induced by OGD, NSP, and NSP + sc3060 processes. Typical star-shaped astrocytes could be observed in the blank control group. No typical astrocytes were observed in the OGD group. We did observe typical star-shaped astrocytes in the OGD12hR24h + NSP group, but not if we added the NF-κB inhibitor, sc3060. B, C, D showed Western blotting analyses of the cytoplasmic lysate and nuclear lysate in the OGD 12h and R24h-treated astrocytes. β-Actin was used as the loading control of the cytoplasmic lysate and histone H3 of the nuclear lysate. (B) p-IKKBα/β (86 kD) was upregulated in OGD 12h and R24h-treated cells (the second array), but downregulated by NSP administration (the third array) and such downregulation was arrested by the NF-κB inhibitor, sc3060 (the fourth array). Analogously, the expression of P65 (the third line, 65 kD) was upregulated in OGD12h and R24 h-treated cells (the second array), but was downregulated by NSP administration (the third array), and such downregulation was again arrested by NF-κB inhibitor, sc3060 (the fourth array). The protein levels of p-IKKBα/β (B) and P65 (C) were enhanced by the OGD 12h and R24h treatment (OGD 12hR24 h vs. blank control), whereas NSP administration significantly inhibited such effects (OGD 12hR24 h vs. OGD12 hR24 h + NSP). The inhibition by NSP significantly recovered after administration of NF-κB inhibitor, sc3060 (OGD12hR24h + NSP vs. OGD12hR24h + NSP + sc3060),* P < 0.05.</p

Potential mechanisms for NSP neuroprotection via the NF-κB pathway.

<p>Red arrows indicate activation. Green arrows indicate inhibition.</p