Female albino mice, on postnatal day 10, were subjected to left carotid artery ligation followed by 8% hypoxia for 25 minutes. During short term experiments three sensorimotor reflexes (Righting, Cliff Aversion and Negative geotaxis) were determined along with brain infarcts to demonstrate the effect of hypoxic-ischemic insult. During long term experiments, mice with and without hypoxic ischemic insult (HI and NO HI) were divided in to three treatments on the basis of diet supplementation (Normal rodent diet, 1% and 3% creatine supplemented diet) for 10 week following weaning on postnatal day 20. A battery of neurological tests was used to asses long term neurofunction (Rota rod, open field and Morris water maze) along with infarct measurement and determination of interleukin-6 and 18 in serum. During short term experiments mice subjected to hypoxia ischemia on postnatal day 10 exhibited poor sensorimotor reflexes 1 and 24 hour after brain injury. During long term experiment, it was observed that overall creatine supplementation in both HI and NO HI group improved neuromuscular performance but the affect was more pronounced in 3% creatine supplemented treatment. In open field, creatine supplementation enhanced locomotory and exploratory behaviour significantly in HI treated mice. During morris water maze it was observed that creatine supplementation improved spatial memory and enhanced swimming speed in both HI and NO HI groups. A significant affect of creatine supplementation in reducing infarct size was also observed. It was noticed that creatine supplementation helped in reducing IL-6 concentrations while no significant effect was observed on IL-18 concentrations in serum of female albino mice during long term experiment following hypoxic ischemic insult. Overall female albino mice supplemented with creatine monohydrate during neurological studies demonstrated better learning abilities and neuromuscular coordination and the affect was more pronounced in HI treated mice. It was also observed that the mice supplemented with 3% creatine diet performed better than mice on 1% creatine diet during series of neurological test batteries in both HI and NO HI group.
2۔قتل شبہ عمد کوئی شخص ، کسی کو ایسے ہتھیار سے مارے جس کی ضرب سے عام طور پر انسان نہیں مرتاجیسے کوڑا ، معمولی ڈنڈالیکن اگر مضروب اس چیز کی ضرب سے مرجاتا ہے تو یہ قتل شبہ عمد ہوگا۔
Qur’an and prophetic traditions (Hadith) are the fundamental sources of Islam. Muslims believe that Qur’an is the word of God (Allah). Hadith (Prophet’s Sayings, actions and silent approvals and disapprovals for something) likewise is based on divine revelation. Qur’an affirms also this view: (God says) Your Companion (Muhammad) has neither gone astray nor has erred. Nor does He speak of (his own) desire. It is only a Revelation revealed. Al-Qur’an (53: 2-4). Allah Almighty Himself took the responsibility to guard His word (the Qur’an): (He says: ) verily, We, it is We Who have sent down the Dhikr (i.e. The Qur’an) and surely, We will got it (from corruption). (Al-Qur’an: 15: 9) on the contrary the responsibility to guard the prophetic traditions (Hadith) was put on the shoulders on the Muslim Ūmmah. The scholars of Islam (ʽulāmʼs) try their utmost to collect and save the Prophetic traditions and guard it from any alteration. To achieve this purpose, they introduced different hadith sciences to distinguished between the true and the fabricated hadith. The authentic Sunnah is contained within the vast body of Hadith literature. Different scholars have compiled the books which contain a large numbers of Ahadith, one of them is ʼimam Taḥāwi. In this article we will discuss the ʼimam Taḥāwi approach towards “Ahadith” in his book Mushkil ul Āathʼar.
The sunshine vitamin is in the limelight for the last couple of years. Though Pakistan is located at favorable latitude and longitude yet vast majority of its people suffer from vitamin D deficiency. Calcium homeostasis, bone metabolism and many other functions of body are influenced by vitamin D. Nuclear vitamin D receptor and group specific vitamin D binding proteins are two important proteins play role in vitamin D metabolism and encoded by VDR and GC genes. There could be many reasons but in this study six single nucleotide polymorphisms in GC, VDR and CYP2R1 genes were looked into for their possible association with vitamin D deficiency. Blood samples of four hundred subjects were collected. Vitamin D and parathyroid harmone levels were calculated by chemiluminescence method. DNA extraction was carried out by phenolchloroform method. The qualitative and quantitative analysis of DNA was carried out on agarose gel electrophoresis. Tetra amplification refractory mutation system polymerase chain reaction was performed to genotype rs7041, rs4588, rs2060793, rs2282679, rs3847987, and rs7974353. Genotypic and allelic frequencies with relative risk was calculated. In Silico protein modelling, docking and analysis of rs7041 was done. Overall 77.5% subjects were found to be with vitamin D deficiency/insufficiency. There were 35% from newborn to 20 years age group, 88.8% from 21-40 years and 95.8% from to 41-60 years.Significant negative correlation was observed between vitamin D and parathyroid hormone levels. rs 7041 belonging to GC genes showed T>G polymorphism. Major allele was T and minor allele was G. Minor allele “G” with genotype GG could be a risk allele contributing in vitamin D deficiency. rs7974353 belonging to VDR gene showed T>A polymorphism. Though “TT’ was in high frequency in VDD subjects compared to control yet insignificant association with VDD was noted. RR for both alleles and genotypes TA and AA was not significant with reference to homozygous wild type TT (0.6 for AT, 0.7 for AA). Results might had been xxi sigificant if thenumber of subjects were more. Rest of the four SNPs showed equal frequency in control and cases and hence showed no association with vitamin D deficiency. In silico model of SNP rs 7041 showed variation in the 3D structure of protein because of replacement of asparctic acid by glutamic acid. This can explain the cause of VDD / VDI due to poor docking of vitamin D with its binding protein. Conclusion is that rs7041 and possibly rs7974353 are contributing to VDD / VDI in studied group. Results are supported by In silico analysis of rs 7041.