A genetic and demographic investigation of the Zoroastrians of Iran.

The aim of this study was to examine the Zoroastrians of Yazd, Kerman and Tehran to determine whether or not they differed from each other genetically and from the host population of Iran; to study the Parsis and Iranis - Zoroastrians Who had migrated to India in the 7th Century A.D., and compare the results with those of neighbouring Indian populations. It was hoped to obtain a large number of samples in order to make accurate comparisons, but, owing to the contemporary complex political situation, this proved impossible. Attempts were made to explain the variants in terms of present day demo graphic theories but were hampered by the paucity of published data. Blood, serum and isoenzyme group examinations were made. Serological and electro0ioretic techniques were used to determine ABo, MNSs, Rh, Kell, Duffy, KP, haptoglobin, adenylate kinase, acid fiiosphatase, esterase D and 0ios0ioglucanutase factors in a total of 469 Zoroastrians. Demographic features of contemporary Zoroastrians were studied and the results compared with those of Iranians and Parsis. (No demographic data was available for the Iranis of India.) This revealed that the fertility ratio of the Zoroastrians is lower and present day infant mortality higher than those for the latter groups. Serological test results together with the demographic findings suggest that the long practise of consanquinial marriage may account for the differences which we can observe today

TGF-β/Smad signaling pathway as a candidate for EMAST phenotype in colorectal cancer patients

Objective: Elevated microsatellite alteration at selected tetranucleotide repeats (EMAST) is a prognostic biomarker in colorectal cancer (CRC). EMAST phenotype appears to be linked to deficiency in DNA mismatch repair (MMR) proteins including MSH3. The TGF-β signaling pathway has a pivotal role in tumorigenesis of CRC. Since the biological causes of EMAST phenomenon has remained a matter of debate, this study aimed to investigate the association between Smad-dependent canonical signaling TGF-β pathway and EMAST phenotype in colorectal cancer patients. Patients and Methods: EMAST status was analyzed in normal and paraffin-embedded tumor tissues of 122 CRC patients using QIAxcel capillary PCR and electrophoresis. Immunohistochemical method was used to determine the expression of canonical TGFβ-signaling pathway and MSH3 proteins. Eventually, the relationship between canonical TGF-β signaling pathway activation and EMAST phenotype and, therefore, MSH3 expression, was evaluated. Results: 40.2% of CRC tumors had EMAST+ phenotype. The canonical TGF-β signaling pathway was activated in 27.9% of patients. Furthermore, 43.4% of patients indicated low expression of MSH3. 64.7% of tumors characterized with activated canonical TGF-β signaling pathway were EMAST+. Finally, a significant relationship between TGF-ß signaling pathway activation and MSH3 expression was observed. Conclusions: In current study, the activation of canonical TGF-β signaling pathway in CRC tumors mediated by Smad proteins was significantly associated with EMAST phenotype and MSH3 expression