The objective of the study is to examine the relationship between money supply, price level and economic growth in the context of Pakistan by using Autoregressive Distributed Lag (ARDL) model, covered a period of 1980 to 2016. The results confirm the long-run relationship between the variables while using broad money supply as a response variable. However, in the price and income modeling, the variables do not support the cointegration relationship between the variables. The causality results confirmed the unidirectional relationship running from income to money supply, which implies that income do causes money supply in the short run, whereas money supply leads to inflation to support Monetarist view of inflation in a country. The results conclude that economic growth is imperative to stabilize money supply and price level through sound economic policies in a country.
This study examined the relationship between savings and investment in the G-7 countries for the period of 1970 to 2015. The stationary analysis of the data has been done by adopting the panel Levin, Lin & Chu, Breitung, Pesaran & Shin, ADF-Fisher & PP-Fisher criteria while the long run relationship has been tested by employing the Pedroni residual test of co-integration. The results neglected the existence of a long run correlation between saving and investment in G-7 countries. Further, joint causality between the savings and investment has also been tested using the fixed effect VAR model. Wald test explains that the two consecutive lags i.e. S (-1) and S (-2) of savings is jointly causing savings in the current year in the G7 countries. While the same two lags of investment i.e. I (-1) and I (-2) does not jointly granger cause savings in the G7 economies. The results are in line with Feldstein and Horioka (1980) that there is a stable and significant association between the increasing rates of savings and investment in the short run while this relationship weaken in the long run.
Background: The participation of endogenous cardiac stem/progenitor cells is limited in restoring cardiac structure and function in the ischemic myocardium which is further aggravated by poor survival and propagation of transplanted stem cells of different origin in the infarcted heart. The goal of this study was to explore the survival and engraftability of newly discovered induced pluripotent stem cells (IPS) in the myocardium following infarction (MI). Methods and Results: Integration free iPS were generated from myoblasts and characterized. Cardiac progenitors (CPs) were created by treatment with a small molecule. CPs proliferation was assessed by BrdU labeling; Differentiation by both RT-PCR and immunofluorescent staining for cardiac markers Nkx2.5, actinin, and -MHC. Gene expression profiling was performed using Affymetrix array. In vivo studies were carried out by injecting CPs or nontreated IPS (3x105), into mouse model of permanent LAD. Echocardiography, histological parameters, TUNEL assay and capillary vessel density were measured 6 weeks post transplantation. Treatment of IPS with a small molecule upregulated Nkx2.5 and maintained up to 4 weeks (p<0.01 vs nontreated IPS). Expression of actinin and -MHC was also detectable at 3 weeks. Increased proliferative activity (p<0.01) evaluated by cell proliferation and Brdu assay was observed. Significant CPs survival and reduced apoptosis were noticed in the small molecule treated iPSC compared to nontreated and/or saline group. Enhanced ejection fraction and fractional shortening (p< 0.05) was observed 6 weeks post transplantation. Interestingly there was 2-3 fold upregulation of chemokines including CCL7, CXCR2, CXCR5. miR Microarray analysis showed upregulation of cardiac specific mir-133,762. Western blot analysis showed increased phospho-Akt levels as compared to nontreated IPSC (p<0.01). Survival and differentiation properties of CPs were abolished by concomitant treatment of IPS with CXR4 blocker (p<0.05). Conclusion: This study provides a novel strategy for generating CPs and their enhanced survival, engraftment and differentiation with the treatment of cardiogenic small molecule post transplantation in the infarcted myocardium through CXCR4 signaling pathway.
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