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مولانا محمد ابوالقاسم سیفؔ بنارسی

مولانا محمد ابوالقاسم سیف بنارسی
افسوس ہے کہ گذشتہ مہینہ جماعتِ اہلحدیث کے مشہور و ممتاز عالم اور نامور مناظر مولانا محمد ابوالقاسم صاحب سیف بنارسی نے ۶۱ سال کی عمر میں انتقال کیا، مرحوم کی ساری عمر دین و علومِ دینیہ کی خدمت میں گذری، مدرسہ سعید یہ بنارس میں چالیس سال تک حدیثِ نبوی کا درس دیا، جوان کی سب سے بڑے فضیلت ہے، درس و تدریس کے ساتھ وعظ و تبلیغ اور تالیف و تصنیف کا شغل بھی تھا، لیکن ان کی بیشتر تصانیف مناظرانہ ہیں، آریوں، عیسائیوں اور قادیانیوں سے بڑے معرکہ کے مناظرے کئے، احناف سے بھی اس کی نوبت آجاتی تھی ادھر چند برسوں کے اندران پر فالج کے کئی ہلکے حملے ہوئے جس سے ان کی صحت بگڑ گئی تھی اس کے باوجود ان کے علمی و تعلیمی مشاغل جاری تھے ، کہ گذشتہ ۲۵؍ نومبر کو جمعہ کے دن پھر اچانک حملہ ہوا اور چند گھنٹوں کے اندر قال اللّٰہ وقال الرسول کی یہ آواز ہمیشہ کے لیے خاموش ہوگئی، مرحوم کے انتقال سے ہندوستان کے طبقہ علماء میں ایک ممتاز جگہ خالی ہوگئی، اللّٰھم اغفرہ مغفرۃً واسعۃً۔ (شاہ معین الدین ندوی، دسمبر ۱۹۴۹ء)

 

ENHANCING REHABILITATION PRACTICES THROUGH ROBUST REGULATION AND INTERDISCIPLINARY COLLABORATION IN PAKISTAN

Rehabilitation forms an important tire in well operating health care systems. Within the areas as mentioned on the World Health Organisation factsheet about rehabilitation the therapeutic professions such as physiotherapists, occupational therapists, speech and language therapists, prosthetists and orthotists and clinical psychologists play an important role. They do not only treat people’s conditions such as diseases, disorders, injuries or trauma, they furthermore promote good health and help to prevent diseases. This can significantly lead to better overall wellbeing of the population. To gain the best client outcome and support the health care system in an effective way, regulation is as important as interprofessional collaboration. Thus there is an intense need to highlight these two main aspects to ensure quality rehabilitation provided by therapeutic professionals.

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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