آخرت سے متعلق ”ترجمان القرآن“ کے کلامی مباحث کا تجزیاتی مطالعہ

In this universe, if we look at the arrival of a human being, it will open up to us the secret that man did not come in this world suddenly, but he had gone through several worlds before stepping into this universe. The First World is called spiritual world where his soul was present and the argument is that when the soul enters the body of the baby and he starts to move in the womb of the mother, so the question now arises where was that soul before it entered the baby’s body? And where did that soul come from? Where it was and wherever it came from, the name of that universe is Spiritual world. After the spiritual world, there is a second world in the womb of the mother. In this world a man must live for at least nine months. Stop for a minute to see this amazing system of power that a baby remains alive in a moving grave for at least nine months. The object is to say that if a human being has to go through two worlds before coming into the universe, so if a fourth world is accepted after this world, what is the rational prohibition behind it? The life in the fourth world is called the life of Hereafter. If there is any disagreement with this name then let’s another name, but a fourth world still have to believe, because when the soul comes out of body after death, the same question will arise here that where did the soul go? In this article, it is examined that how author of “Tarjuman al-Qur’an” Abul Kalam Azad has proved the reality of life of Hereafter and what kind of arguments have given as an evidence in this tafsir?

Pharmacological Screening of Nsaid’S for Their Probable Central Nervous System Effect and Their Role in Neurodegenerative Diseases

Inducible cyclo-oxygenase (COX) expression in the brain is associated with acute neurotoxicity, such as seizures and ischemia. On the other hand COX 1 and 2 both are related to delayed pro-inflammatory activities, which are ought to exacerbate the neuronal damage in neurodegenerative diseases. It was postulated in last decade that non steroidal anti-inflammatory drugs (NSAIDs) which are widely used in clinical situation as anti-inflammatory, analgesics and antipyretic drugs by inhibiting COX pathway in brain can prevent neurodegeneration. However it is still unknown whether NSAIDs have effect on the development on the central nervous system and play a major role to prevent and treat neurodegenerative disease. Previous clinical, epidemiological and experimental data revealed that repeated and long term use of NSAIDs prevent neurodegeneration by inhibiting brain COX isoenzymes and recommended as a new emerging approach. In the present study we aimed to evaluate the effect of diclofenac, ibuprofen and celecoxib on behavioral and biochemical parameters as well as disease severity assessment not only in parkinson’s patients but on chlorpromazine induced parkinson rat model. A single blind clinical study was conducted in four groups of 40 parkinson’s patients. The cognition was measured by MMSE and MoCA test, depression assessed by HDRS test, daily living functioning judged with ADCS-ADL scale and disease severity by Hoehn & Yahr staging and descriptive UPDRS scale. The outcomes were better among patients treated with NSAIDs than control patients. NSAIDs treated patients showed significant improvement in MMSE, MoCA and ADCS-ADL scores after 2 month treatment period from baseline score. However insignificant results were also observed after 2 month treatment with respect to depression and disease severity. The most frequent adverse events during 2 month treatment period were nausea, dyspepsia, elevated hepatic enzymes, and hypertension. NSAIDs showed significant increased SGOT, SGPT, and bilirubin levels but no significant change in GGT and alkaline phosphatase after 2 month treatment was noted. NSAIDs showed significant increased levels of urea and creatinin after 2 month. We found elevated Cortisol levels at baseline in all parkinson patients after taking NSAID we observed slightly reduced levels of cortisol from baseline as compare to control patients but results were insignificant. Behavioral and histopathological examination of NSAIDs treated rats after chlorpromazine induced parkinsonism was observed. NSAIDs were administered after 30 minutes of 3mg/kg ip injection of chlorpromazine up to 21 day. After 21 day we observed significant motor impairment in CPZ treated rat in open field, catalepsy and wire hanging test while NSAIDs treated rat showed significant improvement comparable to standard L-dopa/carbidopa group. NSAIDs treated rats showed significant improved cognitive behaviors in radial arm maze, water maze and passive avoidance test as compare to control and CPZ group. Depression was marked with CPZ group on forced swimming induced test and cage crossing test while NSAIDs treatment improved depression after 21 days. NSAIDs treated rats slightly reduced their weight after 21 days as compare to control and CPZ group while CPZ group significantly increased body weight. Anxiety was assessed by using elevated plus maze. NSAIDs showed anxiety like behavior after 21 day treatment but CPZ treated rats showed anxiolytic effect. Histopathological examination of brain tissue of NSAIDs treated group revealed minimal neuronal destruction and gliosis as compare to CPZ group. In conclusion results of this clinical and experimental study explain that NSAIDs treatment show moderate improvement in parkinson associated cognitive decline, motor impairment and in their daily life function. Adverse drug events were also observed, hence prolong use can only be recommended after extensive study.