تنمية الاسواق المالية وأثرها في الحد من معدلات الفقر دراسة في عينة من البلدان النامية

هدفت الدراسة إلى محاولة تشخيص وتمييز الآثار التي تتركها تنمية الأسواق المالية في الفقر وتفسير آليات انتقال هذا التأثير، سواء بشكل مباشر أو عن طريق النمو الاقتصادي وتباين توزيع الدخل، علاوة على بناء نموذج قادر على تحليل التأثيرات المباشرة وغير المباشرة لتنمية الأسواق المالية في اثنا عشر دولة نامية ستة منها عربية والأخرى دول أجنبية. والأخذ بالاعتبار تقارب مستويات الفقر في تلك الدول للفترة ما بين 2005 إلى 2020 بواقع قراءة لكل خمس سنوات من كل دولة نامية. ولتحقيق ما تقدم استخدمت الدراسة منهجية تحليل المسار (Path Analysis) ونموذج الانحدار الخطي البسيط لغرض تشخيص آلية التأثير التي يمارسها تطور الأسواق المالية في الفقر وبهدف الوصول إلى نتائج أكثر دقة وواقعية، والحصول على تحليل سليم ومنطقي يمكن استخدامه لتوجيه السياسات الاقتصادية والمالية باتجاه محادي للفقراء. واستنتجت الدراسة بأن آليات انتقال تأثير تطور الأسواق المالية تتنوع حسب الأسس التي يستند عليها حيث التأثير ينتقل بشكل متوازن عبر القناة المباشرة أي إن الفائدة تصل بشكل مباشر للفقراء من النظام المالي أو عبر القناة غير المباشرة عبر النمو الاقتصادي وتبيان توزيع الدخل، وانطلاقا مما تقدم يوصى بتوجيه السياسة المالية نحو زيادة الأصول المتداولة وتوسيع شبكة المستثمرين بشكل فعّال، بمنح الشركات في القطاع الخاص الحوافز للمشاركة في الأسواق المالية وتشجيعها على استثمار أموالها في الأسهم والسندات. ومن ثم يجب تعزيز الوصول المتساوي للمستثمرين من مختلف الفئات الاجتماعية إلى الأسواق المالية، من خلال تقديم تسهيلات للمستثمرين وزيادة الاستثمار في التكنولوجيا المالية والتداول عبر الإنترنت. ويُنصح بتبسيط الإجراءات التنظيمية وتحسين البنية التنظيمية للأسواق المالية مع التركيز على تحديث التكنولوجيا لتسهيل المعاملات وخفض التكاليف. وأخيرًا، ينبغي تعزيز الرقابة المالية والحوكمة الإلكترونية وزيادة مستوى الشفافية في عمليات الإفصاح المالي لضمان توفير معلومات دقيقة وموثوقة للمستثمرين، مما سيسهم في تعزيز استقرار الأسواق المالية وزيادة الثقة فيها

Preclinical studies of Apogossypolone: a new nonpeptidic pan small-molecule inhibitor of Bcl-2, Bcl-XL and Mcl-1 proteins in Follicular Small Cleaved Cell Lymphoma model

Elevated expression of anti-apoptotic Bcl-2 family proteins have been linked to a poor survival rate of patients with Follicular Lymphoma (FL). This prompted us to evaluate a very potent non-peptidic Small-Molecule Inhibitor (SMI) targeting Bcl-2 family proteins, Apogossypolone (ApoG2) using follicular small cleaved cell lymphoma cell line (WSU-FSCCL) and cell isolated from lymphoma patients. ApoG2 inhibited the growth of WSU-FSCCL significantly with a 50% growth inhibition of cells (IC50) of 109 nM and decreased cell number of fresh lymphoma cells. ApoG2 activated caspases-9, -3, and -8, and the cleavage of Poly (ADP-ribose) polymerase (PARP) and Apoptosis Inducing Factor (AIF). In the WSU-FSCCL-SCID xenograft model, ApoG2 showed a significant anti-lymphoma effect, with %ILS of 84% in the intravenous and 63% in intraperitoneal treated mice. These studies suggest that ApoG2 can be an effective therapeutic agent against FL

Preclinical studies of Apogossypolone: a new nonpeptidic pan small-molecule inhibitor of Bcl-2, Bcl-X\u3csub\u3eL \u3c/sub\u3eand Mcl-1 proteins in Follicular Small Cleaved Cell Lymphoma model

Abstract Elevated expression of anti-apoptotic Bcl-2 family proteins have been linked to a poor survival rate of patients with Follicular Lymphoma (FL). This prompted us to evaluate a very potent non-peptidic Small-Molecule Inhibitor (SMI) targeting Bcl-2 family proteins, Apogossypolone (ApoG2) using follicular small cleaved cell lymphoma cell line (WSU-FSCCL) and cell isolated from lymphoma patients. ApoG2 inhibited the growth of WSU-FSCCL significantly with a 50% growth inhibition of cells (IC50) of 109 nM and decreased cell number of fresh lymphoma cells. ApoG2 activated caspases-9, -3, and -8, and the cleavage of Poly (ADP-ribose) polymerase (PARP) and Apoptosis Inducing Factor (AIF). In the WSU-FSCCL-SCID xenograft model, ApoG2 showed a significant anti-lymphoma effect, with %ILS of 84% in the intravenous and 63% in intraperitoneal treated mice. These studies suggest that ApoG2 can be an effective therapeutic agent against FL

I-kappa-kinase-2 (IKK-2) inhibition potentiates vincristine cytotoxicity in non-Hodgkin\u27s lymphoma

Abstract Background IKK-2 is an important regulator of the nuclear factor-κB (NF-κB) which has been implicated in survival, proliferation and apoptosis resistance of lymphoma cells. In this study, we investigated whether inhibition of IKK-2 impacts cell growth or cytotoxicity of selected conventional chemotherapeutic agents in non-Hodgkin\u27s lymphoma. Two established model systems were used; Follicular (WSU-FSCCL) and Diffuse Large Cell (WSU-DLCL2) Lymphoma, both of which constitutively express p-IκB. A novel, selective small molecule inhibitor of IKK-2, ML120B (N-[6-chloro-7-methoxy-9H-β-carbolin-8-yl]-2-methylnicotinamide) was used to perturb NF-κB in lymphoma cells. The growth inhibitory effect of ML120B (M) alone and in combination with cyclophosphamide monohydrate (C), doxorubicin (H) or vincristine (V) was evaluated in vitro using short-term culture assay. We also determined efficacy of the combination in vivo using the SCID mouse xenografts. Results ML120B down-regulated p-IκBα protein expression in a concentration dependent manner, caused growth inhibition, increased G0/G1 cells, but did not induce apoptosis. There was no significant enhancement of cell kill in the M/C or M/H combination. However, there was strong synergy in the M/V combination where the vincristine concentration can be lowered by a hundred fold in the combination for comparable G2/M arrest and apoptosis. ML120B prevented vincristine-induced nuclear translocation of p65 subunit of NF-κB. In vivo, ML120B was effective by itself and enhanced CHOP anti-tumor activity significantly (P = 0.001) in the WSU-DLCL2-SCID model but did not prevent CNS lymphoma in the WSU-FSCCL-SCID model. Conclusions For the first time, this study demonstrates that perturbation of IKK-2 by ML120B leads to synergistic enhancement of vincristine cytotoxicity in lymphoma. These results suggest that disruption of the NF-κB pathway is a useful adjunct to cytotoxic chemotherapy in lymphoma

SMI of Bcl-2 TW-37 is active across a spectrum of B-cell tumors irrespective of their proliferative and differentiation status

The Bcl-2 family of proteins is critical to the life and death of malignant B-lymphocytes. Interfering with their activity using small-molecule inhibitors (SMI) is being explored as a new therapeutic strategy for treating B-cell tumors. We evaluated the efficacy of TW-37, a non-peptidic SMI of Bcl-2 against a range spectrum of human B-cell lines, fresh patient samples and animal xenograft models. Multiple cytochemical and molecular approaches such as acridine orange/ethidium bromide assay for apoptosis, co-immunoprecipitation of complexes and western blot analysis, caspase luminescent activity assay and apoptotic DNA fragmentation assay were used to demonstrate the effect of TW-37 on different B-cell lines, patient derived samples, as well as in animal xenograft models. Nanomolar concentrations of TW-37 were able to induce apoptosis in both fresh samples and established cell lines with IC50 in most cases of 165–320 nM. Apoptosis was independent of proliferative status or pathological classification of B-cell tumor. TW-37 was able to block Bim-Bcl-XL and Bim-Mcl-1 heterodimerization and induced apoptosis via activation of caspases -9, -3, PARP and DNA fragmentation. TW-37 administered to tumor-bearing SCID mice led to significant tumor growth inhibition (T/C), tumor growth delay (T-C) and Log10kill, when used at its maximum tolerated dose (40 mg/kg × 3 days) via tail vein. TW-37 failed to induce changes in the Bcl-2 proteins levels suggesting that assessment of baseline Bcl-2 family proteins can be used to predict response to the drug. These findings indicate activity of TW-37 across the spectrum of human B-cell tumors and support the concept of targeting the Bcl-2 system as a therapeutic strategy regardless of the stage of B-cell differentiation

Developments in the efficiency of the Malaysian banking sector: the impacts of financial disruptions and exchange rate regimes

In the mid-1990s, East Asian countries have experienced severe financial crisis that were followed by deep economic downturns. A variety of methodologies have been used to explain the Asian financial crisis. However, the impact of the Asian financial crisis of 1997 on the efficiency of the banking sector has not been studied yet. The present article attempts to provide new empirical evidence on the efficiency of the Malaysian banking sector around the Asian financial crisis. The efficiency estimates of individual banks are evaluated by using the non-parametric data envelopment analysis (DEA) method. The results indicate that the foreign banks have exhibited higher technical efficiency compared to their domestic bank counterparts. However, the results suggest that the foreign banks were severely affected by the Asian financial crisis, implying that the foreign banks are not insulated from unexpected events like the Asian financial crisis of 1997

Saudi-KAU Coupled Global Climate Model: Description and Performance

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Bayesian profiling of molecular signatures to predict event times

BACKGROUND: It is of particular interest to identify cancer-specific molecular signatures for early diagnosis, monitoring effects of treatment and predicting patient survival time. Molecular information about patients is usually generated from high throughput technologies such as microarray and mass spectrometry. Statistically, we are challenged by the large number of candidates but only a small number of patients in the study, and the right-censored clinical data further complicate the analysis. RESULTS: We present a two-stage procedure to profile molecular signatures for survival outcomes. Firstly, we group closely-related molecular features into linkage clusters, each portraying either similar or opposite functions and playing similar roles in prognosis; secondly, a Bayesian approach is developed to rank the centroids of these linkage clusters and provide a list of the main molecular features closely related to the outcome of interest. A simulation study showed the superior performance of our approach. When it was applied to data on diffuse large B-cell lymphoma (DLBCL), we were able to identify some new candidate signatures for disease prognosis. CONCLUSION: This multivariate approach provides researchers with a more reliable list of molecular features profiled in terms of their prognostic relationship to the event times, and generates dependable information for subsequent identification of prognostic molecular signatures through either biological procedures or further data analysis