Among naturally occurring plant growth stimulants, Moringa oleifera has attained enormous attention because of having cytokinin in addition to other growth enhancing compounds like ascorbates, phenolics, other antioxidants along with macro- micro nutrients in its leaves. With these properties, exogenous application of Moringa leaf extract (MLE) was done in wheat, pea and tomato to evaluate its efficacy as crop growth enhancer The objective was to optimize dose, method of exogenous application, enhancement of growth, yield and antioxidant level under normal and abiotic stresses (late sowing, salinity, and drought). The results showed that 30 times diluted MLE priming in wheat under normal conditions was found to be effective. MLE priming improved the seedling emergence rate, speed and early growth and increased level of antioxidants, leaf total soluble protein and chlorophyll contents as compared to MLE10, Hydro priming, On-farm priming and CaCl2 priming. Large number and heavier grains were obtained in plants raised from MLE30 primed seed which resulted in highest grain yield per plant. All the priming treatments gave more yield than non primed control. Foliar spray of MLE caused an increase of 10.73, 6.00, 10.70 and 4.00% in 1000 grain weight, biological yield, grain yield and harvest index respectively, with MLE spray at tillering + jointing + booting + heading. MLE spray only at heading gave 6.84, 3.17, 6.80 and 3.51% more 1000-grain weight, biological yield, grain yield, and harvest index respectively, as compared to control. MLE extended the seasonal leaf area duration (Seasonal LAD) by 9.22 and 6.45 d over control when applied at all growth stages and single spray at heading, respectively. MLE foliar improved salinity tolerance in wheat by improving wheat seedlings vigour, more chlorophyll a and chlorophyll b contents, exclusion of Na+ and Cl- along with accumulation of K+ and larger contents of enzymatic antioxidants (catalase, superoxide dismutase and peroxidase) and non enzymatic antioxidants (ascorbic acid and total phenolic contents) leading to more 100 grain weight as compared to benzylaminpurine (BAP), hydrogen peroxide (H2O2) and control (water spray) under salinity. The water sprayed plants under highest salinity showed maximum accumulation of Na+ and Cl- while largest K+ contents were observed in case of MLE spray under moderate salinity. MLE and BAP application improved leaf total soluble protein and superoxide dismutase (SOD). For non-enzymatic antioxidants (total phenolics and ascorbic acid), MLE was ranked first under moderate salinity. BAP improved number of grains spike-1 but heavier grains were observed under MLE application in moderately saline conditions. These effects of MLE were more apparent under moderate salinity (8dS m-1) as compared to higher salinity (12dS m-1). The water stress caused reduction in growth and grain yield of wheat due to decreased leaf area and reduced chlorophyll a and chlorophyll b contents. However, foliar application of MLE and BAP minimized these effects of drought. MLE application produced more grain yield under moderate and severe water stress as compared to BAP, K+ and control. Moringa leaves being a rich source of β-carotene, protein, vitamin C, calcium and potassium and act as a good source of natural antioxidants such as ascorbic acid, flavonoid, phenolics and carotenoid, so the exogenous applications of MLE improve the antioxidant status and yield of wheat under drought stress. In case of tomato crop foliar application of MLE30 exhibited large number of flowers, more number of fruits as well as heaviest fruits. The foliar application of BAP produced same number of flowers but lighter weight fruits as compared to MLE30. The minimum fruit weight was recorded in case of foliar applied MLE10, MLE0 and control. The effectiveness of MLE as crop growth enhancer might be due to the presence of growth promoting substances. MLE proved a potential growth enhancer in mitigation of abiotic stresses.
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)
Mysticism is the practice of religious ecstasies, together with whatever ideologies, ethics, rights, legends, and magic may be related to them. It may also refer to the attainment of insight in ultimate or hidden truth, and to human transformation supported by various practices and experiences. Sufism also known as Tasawwuf variously defined as Islamic mysticism. The inward dimension of Islam is mysticism in Islam characterized by particular values, ritual practices, doctrines and institutions which began very early in Islamic history and represents "the main manifestation and the most important and central crystallization of mystical practice in Islam. Practitioners of Sufism have been referred to as "Sufis". Sufis have been characterized by their asceticism, especially by their attachment to dhikr, the practice of remembrance of god, often performed after prayers. This article describes of the reality and fact of mysticism, its verbal and literal meanings, and its historical background and also describes its regional division and causes of Tasawwuf. It also analyses of the objections and its answers of which occurred on it.
Background: Prevalence of mild anemia is high in apparently healthy populations in the developing countries of South Asia. A few human studies have shown that use of antioxidant vitamins such as vitamin E could correct anemia. However, the exact molecular mechanism(s) of this correction is still unclear. One of the possible mechanisms of action of vitamin E in enhancing blood hemoglobin levels in humans could be through inhibition of apoptosis of erythroid stem cells. A few studies have shown that the inhibition of proapoptotic proteins by various intra- and extracellular factors may cause increased survival of human erythroid progenitor cells (EPCs). Some of the animal studies have also suggested the possible role of vitamin E in the prevention and/ or correction of defective erythropoiesis. Moreover, it has also been reported that vitamin E decreases the experimentally-induced apoptosis in bone marrow hematopoietic stem cells in animals. The objectives of this study were to find out the effect of vitamin E supplementation on blood hemoglobin levels in apparently healthy but mildly anemic Pakistani adults and to investigate whether any positive effect of vitamin E on hemoglobin levels in apparently healthy humans could be due to inhibition of apoptosis of EPCs. Methods: To study the effect of vitamin E on hemoglobin levels, a single blinded and placebo-controlled trial was carried out on 124 apparently healthy mildly anemic adult human subjects recruited from the General Practioners’ Clinics and also included personnel from the Aga Khan University, Karachi. All the subjects were recruited with informed consent. The study subjects were randomly assigned to the Intervention group (n=82) and the Control group (n=42). In the Intervention group, each subject was given vitamin E (400 mg) every day for three consecutive months, while Control group subjects received a placebo. Eighty six subjects completed the trial. Fasting venous blood was collected at baseline and after three months of supplementation. Blood hemoglobin levels and serum/plasma concentrations of vitamin E, erythropoietin, total antioxidant status (TAS), vitamin B12, folate, ferritin, serum Transferrin Receptor (sTfR), glucose, creatinine and lipid profile were determined, compared between Intervention and Control groups and analyzed using repeated measures ANOVA and multiple linear regression. To find out the probable mechanism of action of vitamin E on blood hemoglobin levels, CD34+-derived EPCs were isolated from human peripheral blood mononuclear cells (PBMNCs) of apparently healthy Pakistani adult volunteers by density gradient centrifugation followed by magnetic activated cell sorting (MACS) using CD34+ selection kit. Purity of the isolated EPCs was assessed through immune fluorescence microscopy using Fluorescein-5-isothiocyanate (FITC)-conjugated monoclonal antibodies against various EPCs surface antigens. The purity of CD34+-derived EPCs was found to be 95-98%. CD34+-derived EPCs were then cultured for 7-14 days in the recommended medium supplemented with erythroid expansion supplement. To study the effect of vitamin E on apoptosis of erythroid stem cells, EPCs were treated in vitro with various concentrations of Tumor necrosis factor (TNF)-α to induce apoptosis. The concentration of TNF-α inducing maximum apoptosis was then selected to study any protective effect of vitamin E. EPCs were then incubated at various concentrations of vitamin E (zero, 10, 50 and 100 μg/ml) or erythropoietin (zero, 10, 50 and 100 IU/ml) followed by addition of 100 ng/ml concentration of TNF-α which produced the maximum apoptosis under the experimental conditions. The percentage of apoptosis of the treated EPCs was measured through flow cytometry by using annexin V and propidium iodide (PI) staining. Two-way ANOVA with replacement was used to find out the mean difference between the effects of increasing concentrations of drug (vitamin E or erythropoietin) treatment and the interaction of these drugs on TNF-α-induced apoptosis of EPCs. Results: In the study population, there was a significant increase in post-supplemental concentrations of both vitamin E and hemoglobin (p value= 0.045 and p value= 0.049, respectively) when compared with their baseline concentrations. However, when the mean post-supplemental levels of both vitamin E and hemoglobin levels were compared, significant increase in vitamin E (p value= 0.01) and hemoglobin (p value <0.001) levels were observed in the intervention group (vitamin E supplemented) as compared to the control (placebo) group. The adjusted regression coefficients (β) and standard error [SE(β)] of the significant determinants of post-supplemental hemoglobin levels were serum concentration of vitamin E (0.983[0.095]), baseline hemoglobin levels (0.768[0.077]), sTfR(-0.06[0.02]) and gender (male or female, -0.656[0.224]). Regarding the second objective of the study pertaining to the possible underlying mechanism of the action of vitamin E on apoptosis of CD34+-derived EPCs, the mean percentages of early and late apoptotic CD34+-derived EPCs after treatment with TNF-α (100 ng/ml) alone were 58.7± 4.87% and 8.9± 3.43%, respectively. Vitamin E and erythropoietin in highest used concentrations (100 μg/ml and 100 IU/ml, respectively) decreased the percent cell early apoptosis of treated EPCs to 25.2± 4.70% and 5.3± 1.81%, respectively. However, there was a significant difference in the mean percentage of TNF-α-induced apoptotic CD34+-derived EPCs in early and late apoptosis by vitamin E treatment (p value= 0.008) which was higher in early as compared to late apoptosis. There was a significant difference in the mean percentage of TNF-α-induced apoptotic CD34+-derived EPCs by vitamin E treatment (p value < 0.001) when analyzed for a statistical interactive effect on early and late apoptotic phases and vitamin E concentration. Conclusion: The study showed a positive role of vitamin E supplementation in improving blood hemoglobin levels in apparently healthy mildly anemic Pakistani adults. The study also showed that one of the possible mechanisms of action of vitamin E appears to be through inhibition of apoptosis of the CD34+-derived EPCs.