Investasi Reksa Dana Dengan Sistem Mudharabah Oleh Pt.bank Syariah Mandiri Pekalongan

Mutual Fund is an organization that works for the small investor to take part in the investment world. Mutual Funds Sharia comes to meet the needs of investors to income derived from the investment of funds could be accounted for religious. Implementation of Shariah Fund has similarities to conventional mutual fund. The basic thing that distinguishes them among other application-contract agreement (engagement) Islam in its operational mechanism. Arrangements regarding the application of the agreement set forth in Sharia Fund DSN-MUI Fatwa No.20/DSNMUI/IV/2001. Under the decree, agreement occurring in Mutual Funds Sharia al-wakalah (representative) and mudaraba (profit sharing). Based on the description, the authors are interested in conducting a study entitled "Mutual Fund Investing System With PT Bank Syariah Mandiri Mudaraba By Pekalongan branch". The formulation of the problem studied, namely: how the application of the Mutual Fund mudaraba PT. Bank Syariah Mandiri branch Pekalongan?, How ahambatan that arise in the application of the principle of mudaraba by PT Bank Syariah Mandiri branch Pekalonagan? This study uses empirical juridical approach is a method research approach to solve the problem denagan conduct research on primary data that exist in the field. On the implementation of Sharia Fund was still bias on a particular understanding of mudaraba system many people are still unfamiliar to the mutual fund products Syariah.hal This has become an important task for the PT. Bank Syariah Mandiri branch Pekalongan to promote products and Shariah Investment Fund meningkatkanya growth based Islamic investment in Indonesia, especially in Islamic Fund

Bioenergetics of the Calf Muscle in Friedreich Ataxia Patients Measured by 31P-MRS Before and After Treatment with Recombinant Human Erythropoietin

<div><p></p><p>Friedreich ataxia (FRDA) is caused by a GAA repeat expansion in the FXN gene leading to reduced expression of the mitochondrial protein frataxin. Recombinant human erythropoietin (rhuEPO) is suggested to increase frataxin levels, alter mitochondrial function and improve clinical scores in FRDA patients. Aim of the present pilot study was to investigate mitochondrial metabolism of skeletal muscle tissue in FRDA patients and examine effects of rhuEPO administration by phosphorus 31 magnetic resonance spectroscopy (31P MRS). Seven genetically confirmed FRDA patients underwent 31P MRS of the calf muscles using a rest-exercise-recovery protocol before and after receiving 3000 IU of rhuEPO for eight weeks. FRDA patients showed more rapid phosphocreatine (PCr) depletion and increased accumulation of inorganic phosphate (Pi) during incremental exercise as compared to controls. After maximal exhaustive exercise prolonged regeneration of PCR and slowed decline in Pi can be seen in FRDA. PCr regeneration as hallmark of mitochondrial ATP production revealed correlation to activity of complex II/III of the respiratory chain and to demographic values. PCr and Pi kinetics were not influenced by rhuEPO administration. Our results confirm mitochondrial dysfunction and exercise intolerance due to impaired oxidative phosphorylation in skeletal muscle tissue of FRDA patients. MRS did not show improved mitochondrial bioenergetics after eight weeks of rhuEPO exposition in skeletal muscle tissue of FRDA patients.</p><p>Trial Registration</p><p><i>EU Clinical Trials Register</i><a href="https://www.clinicaltrialsregister.eu/ctr-search/trial/2008-000040-13/AT" target="_blank">2008-000040-13</a></p></div

Demographics and concentration of metabolites.

<p>Demographical and clinical values of FRDA patients before (<i>FRDA baseline</i>) and after stimulation (<i>FRDA rhuEPO</i>) with rhuEPO shown as comparison to healthy control subjects (<i>Controls</i>). Absolute concentrations of metabolites (PCr, Pi) in resting state, at exercise abruption and at the end of regeneration are given as mmol/l by using ATP as an internal standard. Intracellular pH was calculated from the chemical shift of Pi.</p><p><i>Values are given as mean and standard deviation (SD). Abbreviations: SARA (scale for the assessment and rating of ataxia), Repeats (GAA repeat of the shorter allele is given), Duration (disease duration), PCr (phosphocreatine), Pi (inorganic phosphate), FRDA (Friedreich ataxia), rhuEPO (recombinant human erythropoietin</i>).</p

Phosphocreatine and inorganic phosphate kinetics.

<p>Time course of phosphocreatine (PCr) and inorganic phosphate (Pi) are shown during exercise in increment 1 and recovery period after maximal exhaustive exercise. Curves are shown as a comparison of healthy controls (<i>dashed curves</i>) to treatment naïve FRDA patients at baseline (<i>solid curves</i>) and FRDA patients after rhuEPO administration (<i>dotted curves</i>). Values are given as a function of time (x) in percentage of changes in PCr and Pi from baseline of the respective increment (100%) and are based on the asymptotic exponential regression model </p