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مختارات من رباعيات مولانا جلال الدين الرومي
إذا أردت الوعي بالواحد المطلق بعد أن أضعت نفسك في التقاليد الهندية، وأردت رؤية أجمل الطهارة والسمو، فعليك الانتقال إلى شعراء الإسلام، حينما يضع جلال الدين الرومي الرائع تركيزا خاصا على وحدة النفوس مع الواحد في المحبة، وهذه الوحدانية الروحية تسمو فوق المحدود والشائع \". إن هيجل في تقييمه يرى أن الرومي يعطي تفسيرا لما هو طبيعي وروحي حيث يتم فصل الضحالة والتفاهة من الطبيعة المجردة ويتم استيعابها في التجربة والتأمل في العالم الروحي ليستمر بمقارنتها بنوع آخر من وحدة الوجود مدعومة بفلسفتي زيون الايلي و سبينوزا\".فالشاعر المسلم كما يرى هيجليسعى إلى استشفاف الإلهي في الأشياء المخلوقة كلها، وحين يستشفه فيها كلها، فان الشاعر يتخلى عن ذاته لكي يعقل في الوقت ذاته أي يدرك أن الله في داخله، بمعنى أن يرى الله في نفسه هو، وهذا ما يعود عليه بجوانب باطنية صافية، وسعادة حرة حين يتخلى عن خصوصيته الذاتية الفردية ليستغرق في الله الأزلي المطلق، وهذا الاستغراق وهذه الحياة التي ملؤها البهجة والغبطة هي التصوف ولذا نجد أن الحب الذي يفرزه شعر جلال الدين الرومي يعبر فيه عن الإنسان الذي يستغرقه حب الله فيرى كل شيء مغمورابهذا الحب.
Book
TGF-β induces miR-100 and miR-125b but blocks let-7a through LIN28B controlling PDAC progression
TGF-β/Activin induces epithelial-to-mesenchymal transition and stemness in pancreatic ductal adenocarcinoma (PDAC). However, the microRNAs (miRNAs) regulated during this response have remained yet undetermined. Here, we show that TGF-β transcriptionally induces MIR100HG lncRNA, containing miR-100, miR-125b and let-7a in its intron, via SMAD2/3. Interestingly, we find that although the pro-tumourigenic miR-100 and miR-125b accordingly increase, the amount of anti-tumourigenic let-7a is unchanged, as TGF-β also induces LIN28B inhibiting its maturation. Notably, we demonstrate that inactivation of miR-125b or miR-100 affects the TGF-β-mediated response indicating that these miRNAs are important TGF-β effectors. We integrate AGO2-RIP-seq with RNA-seq to identify the global regulation exerted by these miRNAs in PDAC cells. Transcripts targeted by miR-125b and miR-100 significantly overlap and mainly inhibit p53 and cell–cell junctions’ pathways. Together, we uncover that TGF-β induces an lncRNA, whose encoded miRNAs, miR-100, let-7a and miR-125b play opposing roles in controlling PDAC tumourigenesis.
In pancreatic ductal adenocarcinoma, TGF-β/Activin induce epithelial-to-mesenchymal transition (EMT) and stemness. Here, the authors show that TGF-β induces pro-tumourigenic miR-100 and miR-125b, but blocks anti-tumourigenic let-7a maturation via LIN28B, regulating pathways to promote stemness, EMT and tumourigenesis.
Journal Article
الحركة العلمية في أثناء موسم الحج حتى عام 656هـ / 1258م : (العلوم الإنسانية)
احتوى الكتاب على فصلين ومقدمة، فقد تناول الفصل الأول علوم اللغة وآدابها وعلم التاريخ، وافرد الفصل الثاني للحديث عن علم الجغرافية والرحلات العلمية. وناقش الكتاب أن الحج كفريضة إسلامية ساهمت في نشر الحركة العلمية في أقطار وأقاليم العالم الإسلامي، واستمرت هذه الحركة محتفظة بقوتها وتجددها في كل موسم. وبين الكتاب أن فريضة الحج لم تكن فريضة دينية فقط، بل أقرنت بالكثير من المقاصد منها طلب العلم والاستزادة منه، إذ كان حضور العلماء وطلبة العلم في مكان وزمان واحد خلق بيئة علمية، ومسرحا للتبادل الثقافي والفكري ومحطة للتزود العلمي، التي أحدثت انعكاسات إيجابية على الحضارة الإسلامية والحياة العلمية.
Book
Efferocytosis induces a novel SLC program to promote glucose uptake and lactate release
Development and routine tissue homeostasis require a high turnover of apoptotic cells. These cells are removed by professional and non-professional phagocytes via efferocytosis
1
. How a phagocyte maintains its homeostasis while coordinating corpse uptake, processing ingested materials and secreting anti-inflammatory mediators is incompletely understood
1
,
2
. Here, using RNA sequencing to characterize the transcriptional program of phagocytes actively engulfing apoptotic cells, we identify a genetic signature involving 33 members of the solute carrier (SLC) family of membrane transport proteins, in which expression is specifically modulated during efferocytosis, but not during antibody-mediated phagocytosis. We assessed the functional relevance of these SLCs in efferocytic phagocytes and observed a robust induction of an aerobic glycolysis program, initiated by SLC2A1-mediated glucose uptake, with concurrent suppression of the oxidative phosphorylation program. The different steps of phagocytosis
2
—that is, ‘smell’ (‘find-me’ signals or sensing factors released by apoptotic cells), ‘taste’ (phagocyte–apoptotic cell contact) and ‘ingestion’ (corpse internalization)—activated distinct and overlapping sets of genes, including several SLC genes, to promote glycolysis. SLC16A1 was upregulated after corpse uptake, increasing the release of lactate, a natural by-product of aerobic glycolysis
3
. Whereas glycolysis within phagocytes contributed to actin polymerization and the continued uptake of corpses, lactate released via SLC16A1 promoted the establishment of an anti-inflammatory tissue environment. Collectively, these data reveal a SLC program that is activated during efferocytosis, identify a previously unknown reliance on aerobic glycolysis during apoptotic cell uptake and show that glycolytic by-products of efferocytosis can influence surrounding cells.
Distinct transcriptional programs are activated during different stages of apoptotic cell engulfment, including a unique program of genes coding for solute carrier proteins and enzymes in the glycolytic pathway.
Journal Article
الحياة الجديدة : فيتا نووفا
التقى دانتي بياتريشي، في مدينة فلورنسة وهو ينهي عامة التاسع، وكانت هي تدخل عامها التاسع (واسمها الحقيقي بيتشي دي فولكو بورتيناري، تزوجت من سيموني دي باردي وتوفيت في سن السادسة والعشرين). نحن لا نعلم إلا القليل عن قصة الحب التي جمعت الشاعر وملهمته، والتي رفع من شأنها كتاب \"فيتا نووفا\"، الذي يرجح أكثر من مؤرخ أنه كتب بين 1292 و1293. هذا الكتاب الذي ظل حتى القرن التاسع عشر \"ضحية\" الكوميديا الإلهية في \"فيتا نووفا\" يصف دانتي حبه العارم لبياتريشي، وحزنه العميق على موتها والأزمة التي عاشها على إثر موتها، وتيهه.
Book
Mannose impairs tumour growth and enhances chemotherapy
It is now well established that tumours undergo changes in cellular metabolism
1
. As this can reveal tumour cell vulnerabilities and because many tumours exhibit enhanced glucose uptake
2
, we have been interested in how tumour cells respond to different forms of sugar. Here we report that the monosaccharide mannose causes growth retardation in several tumour types in vitro, and enhances cell death in response to major forms of chemotherapy. We then show that these effects also occur in vivo in mice following the oral administration of mannose, without significantly affecting the weight and health of the animals. Mechanistically, mannose is taken up by the same transporter(s) as glucose
3
but accumulates as mannose-6-phosphate in cells, and this impairs the further metabolism of glucose in glycolysis, the tricarboxylic acid cycle, the pentose phosphate pathway and glycan synthesis. As a result, the administration of mannose in combination with conventional chemotherapy affects levels of anti-apoptotic proteins of the Bcl-2 family, leading to sensitization to cell death. Finally we show that susceptibility to mannose is dependent on the levels of phosphomannose isomerase (PMI). Cells with low levels of PMI are sensitive to mannose, whereas cells with high levels are resistant, but can be made sensitive by RNA-interference-mediated depletion of the enzyme. In addition, we use tissue microarrays to show that PMI levels also vary greatly between different patients and different tumour types, indicating that PMI levels could be used as a biomarker to direct the successful administration of mannose. We consider that the administration of mannose could be a simple, safe and selective therapy in the treatment of cancer, and could be applicable to multiple tumour types.
Mannose reduces the growth of tumour cells by impairing the metabolism of glucose, and enhances cell death when used in combination with conventional chemotherapy.
Journal Article
Adaptable haemodynamic endothelial cells for organogenesis and tumorigenesis
Endothelial cells adopt tissue-specific characteristics to instruct organ development and regeneration
1
,
2
. This adaptability is lost in cultured adult endothelial cells, which do not vascularize tissues in an organotypic manner. Here, we show that transient reactivation of the embryonic-restricted ETS variant transcription factor 2 (ETV2)
3
in mature human endothelial cells cultured in a serum-free three-dimensional matrix composed of a mixture of laminin, entactin and type-IV collagen (LEC matrix) ‘resets’ these endothelial cells to adaptable, vasculogenic cells, which form perfusable and plastic vascular plexi. Through chromatin remodelling, ETV2 induces tubulogenic pathways, including the activation of RAP1, which promotes the formation of durable lumens
4
,
5
. In three-dimensional matrices—which do not have the constraints of bioprinted scaffolds—the ‘reset’ vascular endothelial cells (R-VECs) self-assemble into stable, multilayered and branching vascular networks within scalable microfluidic chambers, which are capable of transporting human blood. In vivo, R-VECs implanted subcutaneously in mice self-organize into durable pericyte-coated vessels that functionally anastomose to the host circulation and exhibit long-lasting patterning, with no evidence of malformations or angiomas. R-VECs directly interact with cells within three-dimensional co-cultured organoids, removing the need for the restrictive synthetic semipermeable membranes that are required for organ-on-chip systems, therefore providing a physiological platform for vascularization, which we call ‘Organ-On-VascularNet’. R-VECs enable perfusion of glucose-responsive insulin-secreting human pancreatic islets, vascularize decellularized rat intestines and arborize healthy or cancerous human colon organoids. Using single-cell RNA sequencing and epigenetic profiling, we demonstrate that R-VECs establish an adaptive vascular niche that differentially adjusts and conforms to organoids and tumoroids in a tissue-specific manner. Our Organ-On-VascularNet model will permit metabolic, immunological and physiochemical studies and screens to decipher the crosstalk between organotypic endothelial cells and parenchymal cells for identification of determinants of endothelial cell heterogeneity, and could lead to advances in therapeutic organ repair and tumour targeting.
The transient reactivation of ETV2 in adult human endothelial cells reprograms these cells to become adaptable vasculogenic endothelia that in three-dimensional matrices self-assemble into vascular networks that can transport blood and physiologically arborize organoids and decellularized tissues.
Journal Article
The emergent landscape of the mouse gut endoderm at single-cell resolution
Here we delineate the ontogeny of the mammalian endoderm by generating 112,217 single-cell transcriptomes, which represent all endoderm populations within the mouse embryo until midgestation. We use graph-based approaches to model differentiating cells, which provides a spatio-temporal characterization of developmental trajectories and defines the transcriptional architecture that accompanies the emergence of the first (primitive or extra-embryonic) endodermal population and its sister pluripotent (embryonic) epiblast lineage. We uncover a relationship between descendants of these two lineages, in which epiblast cells differentiate into endoderm at two distinct time points—before and during gastrulation. Trajectories of endoderm cells were mapped as they acquired embryonic versus extra-embryonic fates and as they spatially converged within the nascent gut endoderm, which revealed these cells to be globally similar but retain aspects of their lineage history. We observed the regionalized identity of cells along the anterior–posterior axis of the emergent gut tube, which reflects their embryonic or extra-embryonic origin, and the coordinated patterning of these cells into organ-specific territories.
The developing mouse gut endoderm, mapped at single-cell resolution, reveals trajectories of cell differentiation before and during gastrulation and the emergence of regionalized cell identities along the anterior–posterior axis of the gut tube.
Journal Article