دور الإنفاق في سبیل اللہ في رفاھیة المجتمع المعاصر في ضوء فقه السیرۃ

Spending in the cause of Allh is one of the most important ways for the welfare of society and all the divine books agreed about its vital role in the betterment of human lives. But it is obvious from Quraan that not everyone has capacity for it but only those who are saved from stinginess: And whoever is protected from the stinginess of his soul - it is those who will be the successful. (Al-Hashr: 09) It is also very relevant question in this regard that what should be spent? And how and where should be spent? Hence only that type of spending which is according to the need of time is worthy to be called as best use of it, as Prophet (Peace be upon Him) pointed out to the charity of water when Saad ibn e ubadah asked him about the best mean of charity after the death of his mother and people were in urgent need of water. So it is clear that the one who intended to charity must have the actual and original idea about the demand of those who are in crises and then he should decide to arrange the appropriate means in this regard. We found crystal clear indications in the seerat ur rasool (Peace be upon Him) about the appropriate spending in accordance with the demands of current time like the encouraging the release of slaves especially in the Makkah and the treaty of brotherhood among the immigrants and the ansaar and promoting the building of prophetic mosque and preparing the army for battles and promising the abode in paradise in response. This article deals with role of charity in welfare of current society by the proper means and ways, some of the important points are as follows: 1. Introduction. 2. Importance of Infaq in Quraan and Sunnah. 3. Examples of charity in accordance with the demands of society in light of seerah. 4. Charity endowments and its role in the well-being of society in the light of fiqh us seerah. 5. The needs of contemporary society and the role of Charity endowments. 6. Pre-protection from negativity, because prevention is better than cure. 7. Recommendations or proposals for proper expenditure

Role of Hepatitis-C Virus Non Structural Proteins in the Induction of Insulin Resistance

Hepatitis C Virus is one of the lethal infections prevailing throughout the world. There are approximately 8.5 million individuals that are infected with this deadly virus in Pakistan. Hepatitis C virus is responsible for acute and chronic viral infection. Chronic hepatitis C virus infection causes persistent inflammation that leads to liver fibrosis, insulin resistance/type 2 diabetes mellitus, liver cirrhosis and finally hepatocellular carcinoma (HCC). There is strong evidence that insulin resistance has a major role in metabolic syndrome, and is a risk factor for increased liver fibrosis in patients with chronic hepatitis C virus infection. However the underlying mechanism of insulin resistance in chronic hepatitis C virus infection is not well known. The present study describes the molecular mechanism of HCV nonstructural protein 5A (NS5A) induced insulin resistance. In this study, we elucidated the molecular mechanism involved in HCV nonstructural protein 5A (NS5A) induced insulin resistance. In the present study human hepatoma cell line Huh 7.5 was transfected with HCV NS5A (Huh 7.5/NS5A) as well as HCV (JFH-1) genomic RNA was transfected into Huh 7.5 cell line (Huh 7.5/HCV) to discern the effect of HCV and HCV NS5A protein upon modulation of insulin signaling pathway. Here, we demonstrated that an increased serine phosphorylation of insulin receptor substrate-1 (pSer307) and Akt (pSer473) in Huh 7.5/HCV infected cells compared to mock infected cells. Interestingly, the Huh 7.5/NS5A cell line showed an increased serine phosphorylation of pSer307 IRS-1 and pSer473 Akt, compared to the mock transfected cells, which is a critical step defining the downstream insulin signaling pathway. Glycogen synthase kinase-3 (GSK-3), the downstream target of Akt, is known to favor gluconeogenesis. Our results revealed a diminished phosphorylation level of GSK-3 in Huh 7.5/NS5A expressing hepatoma cells compared to the mock transfected cells, thereby favoring gluconeogenesis. Forkhead transcription factor (FOX-01) which is another important downstream target of insulin signaling pathway, was shown to undergo reduced phosphorylation level (pSer 256) in Huh 7.5/NS5A expressing hepatoma cells compared to the mock transfected cells. Collectively, these findings suggest a molecular mechanism by which ectopic expression of Huh 7.5/NS5A modulates the insulin signaling pathway at post translational level. There are several gluconeogenic and lipogenic markers lying downstream to the insulin mediated signaling molecules (pSer307IRS-1, pSer473Akt, pSer256Fox-01 and GSK-3). In this study, we observed that Huh 7.5/HCV infected hepatoma cells as well as ectopic expression of Huh 7.5/NS5A leads to enhanced gluconeogenesis through up regulating the mRNA levels of gluconeogenic genes i.e. Phosphoenol pyruvate carboxy kinase (PEPCK) and Glucose-6-phosphatase (G6P) compared to their controls. In the similar way, an elevated mRNA level of Diacyl glycerol acyltransferase (DGAT), a key lipogenic marker, was also observed in Huh 7.5/HCV infected as well as Huh 7.5/NS5A expressing hepatoma cells compared to their controls. Based on these results, we deduce a mechanism through which HCV NS5A is potentially capable of modulating the entire insulin signaling pathway at mRNA and post-translational level thereby paving a way towards insulin resistance, a metabolic syndrome.