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76. Al-Insan/The Human Being

76. Al-Insan/The Human Being

I/We begin by the Blessed Name of Allah

The Immensely Merciful to all, The Infinitely Compassionate to everyone.

76:01
a. Was there not a time in the past when the human being was nothing even to be mentioned?!

76:02
a. Indeed, it is WE WHO created human being of a drop of the mingling of seminal and
ovarian fluid of male and female, so that WE may test him during his lifetime.
b. Then WE enabled him with hearing and seeing and intellect.

76:03
a. And WE guided him on to the Right Path
b. to see whether he be grateful by following the Right Path, or be ungrateful by straying off the Right Path.

76:04
a. WE have definitely prepared for the ungrateful - by being sinful - chains and shackles and
a blazing fire.

76:05
a. As for the grateful - by being righteous - they will drink from cups containing a mixture of camphor/musk -

76:06
a. from a spring at which the servants of Allah will drink,
b. - making it gush out abundantly.

76:07
a. The righteous are the ones who used to fulfill their vows, and
b. stand in awe of the Time the evil of which will be encompassing everyone.

76:08
a. And they - the righteous – used to give food
- to the needy, for the love of HIM,
- and also to the orphan,
- and to the captive/prisoner of war,

700 Surah 76 * Al-Insan

76:09
a. saying within themselves:
b. ‘We feed you only for the Face...

برما میں روہنگیا مسلمانوں کے مذہبی مسائل اور اس کے اسباب و اثرات

Buddhism is dominated by such other characteristics as sympathy, pity, and kindness. Furthermore, it forbids all kind of cruelty, violence, murder, brutality, and giving pain to any living creature. However, contrary to his teachings, the way his followers have targeted the Rohingya Muslims with violence and atrocities only shows how little they follow Gautama Buddha. Right from the independence of Burma, Buddhists,  declaring Muslims as a threat, started their genocide, which involved attacking their mosques, their homes, dishonoring Muslim women, and harassing the Muslims without any reason. This compelled Muslims to leave their homes and migrate. The recent wave of violence, starting in June 2012,  seriously affected the Muslim majority province of Arakan. Keeping in mind, Arakan is one of the fourteen Burmese provinces, where Islam have ruled since the time of Isalmic Caliphate. Unfortunately, in 1784, Burmese Prince Bodo Phia violated this garden of Islam by carrying out Muslim genocide. He banned all symbols of Islam such as pilgrimage, sacrifice,  prayers, Friday and Eid Prayers, and preaching. This study points out the religious problems and issues of Muslims believers in Arakan including its impact, causes and consequences on their lives. The analytical research Methodolgy has been adopted in this studty.

Modelling of Tlr4 and Jak/Stat Signalling Pathways and Protein-Protein Interaction Studies to Examine the Pathophysiology of Sepsis

In this thesis, the medical condition of sepsis is considered at molecular level (signalling pathways) using computational systems-level approaches in order to get insights into the mechanism of disease progression. Sepsis is the pathological condition provoked due to the presence of bacterial endotoxin in the bloodstream. Subsequently Toll like receptors (TLR)4 and JAK/STAT signalling pathways attempt to reduce the pathogen burden by inducing pro- and anti-inflammatory innate immune responses. However, in some instances, an overwhelmed immune system could not properly regulate the balance between infection and inflammation that may ultimately lead to organ damage and consequently to death. In recent years, there has been an increasing amount of literature on the pattern of pro- and anti-inflammatory response elicited during sepsis, though; there has been a little agreement on the roles of pro- and antiinflammatory cytokines (AiCyts) in sepsis. This study mainly aims to address the controversy behind roles of pro- and anti-inflammatory cytokines in sepsis by modelling the signalling pathway of TLR4 and one of the connected signalling cascades of JAK/STAT using qualitative modelling approach introduced by René Thomas’. The possible system dynamics of TLR4-JAK/STAT signalling pathways are produced for two medical conditions i.e. non-sepsis (type of infections that generally do not cause sepsis) and sepsis along with perturbations in these two cases. As a result, recurrent induction and inactivation of pro-inflammatory cytokines is found as the basic feature associated with sepsis. Besides AiCyts, IFN-β and SOCS-1 are found to mediate down-regulation of pro-inflammatory cytokines at different stages of signalling which cause variation of pro-inflammatory cytokines levels. It is observed that intervention in IFN-β mediated down-regulation of pro-inflammatory cytokines at earlier stages of system dynamics, while intervening the SOCS-1 mediated down-regulation of proinflammatory cytokines at later stages ensures hyper-inflammatory condition. On the other hand, interventions in TLR4, NFκB (transcription factor involved in the TLR4 1 Abstract signalling pathway) and JAK/STAT signalling are good choices for supporting the anti-inflammatory immune responses. Thus only possible protein-protein interactions involved in the initial downstream interactions of TLR4 signalling are studied in order to predict a more appropriate target in these interactions. Previous studies indicated that MyD88 adaptor-like protein (MAL) is an endogenous adaptor protein recognized as an important protein involved in the induction of TLR4 mediated downstream signalling pathway. Moreover, it has also been demonstrated that BTK and PKCδ phosphorylate MAL (positions Tyr86 and Tyr106) which ultimately activates MAL. Thus the modelling of PKCδ and protein-protein interactions of both BTK and PKCδ with MAL is performed in order to explore their competitive interaction. Molecular docking and physicochemical analysis reveals that PKCδ may phosphorylate only Tyr106 of MAL, while BTK may phosphorylate MAL at both positions. Interestingly, the charge and hydrophobicity at interfaces of PKCδ and BTK are found different in nature yet well-compatible with the individual positions of Tyr86 and Tyr106 of MAL. The most prominent findings emerged from this analysis is that position Tyr86 of MAL may explicitly be phosphorylated by BTK, while position Tyr106 of MAL may be phosphorylated by the competing interest of both PKCδ and BTK. In conclusion, this thesis will enhance our understanding about the signalling and protein-protein interactions involved in sepsis which will contribute to the development of drugs and vaccines against the medical condition of sepsis.
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