The 'four principles of bioethics' as found in 13(th) century Muslim scholar Mawlana's teachings

BACKGROUND: There have been different ethical approaches to the issues in the history of philosophy. Two American philosophers Beachump and Childress formulated some ethical principles namely 'respect to autonomy', 'justice', 'beneficence' and 'non-maleficence'. These 'Four Principles' were presented by the authors as universal and applicable to any culture and society. Mawlana, a great figure in Sufi tradition, had written many books which not only guide people how to worship God to be close to Him, but also advise people how to lead a good life to enrich their personality, as well as to create a harmonious society and a peaceful world. METHODS: In this study we examined the major works of Mawlana to find out which of these 'Four Principles of Bioethics' exist in Mawlana's ethical understanding. RESULTS: We have found in our study that all these principles exist in Mawlana's writings and philosophy in one form or another. CONCLUSIONS: We have concluded that, further to Beachump and Childress' claim that these principles are universal and applicable to any culture and society, these principles have always existed in different moral traditions in different ways, of which Mawlana's teaching might be presented as a good example

High Frequency of Endothelial Colony Forming Cells Marks a Non-Active Myeloproliferative Neoplasm with High Risk of Splanchnic Vein Thrombosis

Increased mobilization of circulating endothelial progenitor cells may represent a new biological hallmark of myeloproliferative neoplasms. We measured circulating endothelial colony forming cells (ECFCs) in 106 patients with primary myelofibrosis, fibrotic stage, 49 with prefibrotic myelofibrosis, 59 with essential thrombocythemia or polycythemia vera, and 43 normal controls. Levels of ECFC frequency for patient's characteristics were estimated by using logistic regression in univariate and multivariate setting. The sensitivity, specificity, likelihood ratios, and positive predictive value of increased ECFC frequency were calculated for the significantly associated characteristics. Increased frequency of ECFCs resulted independently associated with history of splanchnic vein thrombosis (adjusted odds ratio = 6.61, 95% CI = 2.54–17.16), and a summary measure of non-active disease, i.e. hemoglobin of 13.8 g/dL or lower, white blood cells count of 7.8×109/L or lower, and platelet count of 400×109/L or lower (adjusted odds ratio = 4.43, 95% CI = 1.45–13.49) Thirteen patients with splanchnic vein thrombosis non associated with myeloproliferative neoplasms were recruited as controls. We excluded a causal role of splanchnic vein thrombosis in ECFCs increase, since no control had elevated ECFCs. We concluded that increased frequency of ECFCs represents the biological hallmark of a non-active myeloproliferative neoplasm with high risk of splanchnic vein thrombosis. The recognition of this disease category copes with the phenotypic mimicry of myeloproliferative neoplasms. Due to inherent performance limitations of ECFCs assay, there is an urgent need to arrive to an acceptable standardization of ECFC assessment

JAK2 GGCC haplotype in MPL mutated myeloproliferative neoplasms.

JAK2 (V617F) is associated with a genetic predisposition to its acquisition, as it is preferentially found in subjects with a common constitutional JAK2 haplotype known as 46/1 or GGCC. A recent study suggests that a genetic predisposition to acquisition of MPL mutation may exist in sporadic patients, since an association was found with the JAK2 46/1 haplotype. We genotyped 509 patients with myeloproliferative neoplasms (MPN), 7% of which carrying a somatic mutation of MPL Exon 10. We found that the JAK2 GGCC haplotype was closely associated with JAK2 (V617F) (OR 1.84, P < 0.001) but not with MPL mutations (OR 0.98), suggesting a different genetic background for these molecular lesions

LNK mutations in familial myeloproliferative neoplasms.

Germ line LNK mutations rarely occur in familial MPNs and do not segregate with the disease phenotype. Our findings suggest that mutations in LNK, either germ line or acquired, may cooperate with acquired driver mutations in JAK2, CALR, or MPL to determine disease phenotype in MPNs

Increased risk of thrombosis in JAK2 V617F-positive patients with primary myelofibrosis and interaction of the mutation with the IPSS score

we provided evidence that PMF patients have a relevant and life-threatening risk of thrombosis and that the lower-risk IPSS categories (low/intermediate-1) harboring the JAK2 V617F mutation are at the highest risk. In clinical practice, this risk could justify studies testing primary prophylaxis with low-dose aspirin in all positive JAK2 V617F patients, particularly in those with lower-risk IPSS scores, if not otherwise contraindicated

JAK2 or CALR mutation status defines subtypes of essential thrombocythemia with substantially different clinical course and outcomes.

Patients with essential thrombocythemia may carry JAK2 (V617F), an MPL substitution, or a calreticulin gene (CALR) mutation. We studied biologic and clinical features of essential thrombocythemia according to JAK2 or CALR mutation status and in relation to those of polycythemia vera. The mutant allele burden was lower in JAK2-mutated than in CALR-mutated essential thrombocythemia. Patients with JAK2 (V617F) were older, had a higher hemoglobin level and white blood cell count, and lower platelet count and serum erythropoietin than those with CALR mutation. Hematologic parameters of patients with JAK2-mutated essential thrombocythemia or polycythemia vera were related to the mutant allele burden. While no polycythemic transformation was observed in CALR-mutated patients, the cumulative risk was 29% at 15 years in those with JAK2-mutated essential thrombocythemia. There was no significant difference in myelofibrotic transformation between the 2 subtypes of essential thrombocythemia. Patients with JAK2-mutated essential thrombocythemia and those with polycythemia vera had a similar risk of thrombosis, which was twice that of patients with the CALR mutation. These observations are consistent with the notion that JAK2-mutated essential thrombocythemia and polycythemia vera represent different phenotypes of a single myeloproliferative neoplasm, whereas CALR-mutated essential thrombocythemia is a distinct disease entity