Gujarat
In Gujarat, most of the Sayyid families are descended from individuals invited by the Muslim rulers of Gujarat to serve as advisers and administrators, and were granted jagirs. During the period of Sultan Mahmud Begada (1458–1511), the sultan provided land to three Sayyid brothers and a grant to settle there after the victory of Pavagadh Fort. In 1484 the sultan conquered the fort on 21 November 1484 and transferred his capital to Champaner, which he completely rebuilt at the foothills of the Pavagadh Fort and named it Muhammadabad. During Mughal rule in Gujarat (1570–1750), the Sayyid held the majority of the civil and ecclesiastical posts. For example, the Sayyids of Thasra, Kheda district, were invited to serve as administrators and judges by the Mughal Emperor, Aurangzeb, and were provided land grants to settle there. They also comprised a significant portion of the Mughal army, and many are still found in old Muslim garrison towns like Ahmedabad. Many of the early Sufi saints that came to Gujarat belonged to Sayyid families, most of which came from Central Asia, Iran, Yemen, Oman, Basra, and Bahrain. South India
Kerala
Thangals, a social group in among the Muslims of Kerala (most whom follow the Shafii madhab), are roughly equivalent to the Sayyids. The thangal families are numerous in Kerala. Most members of the community practices endogamy and some are considered as saints. Thangal families have many gradations of status on social and economic scale. Influential of the thangals generally come from prominent business families.
Fanconi anaemia (FA) is a rare genetic disease resulting in impaired response to DNA damage. Although it is a very rare disorder, study of this and other bone marrow failure syndromes has improved scientific understanding of the mechanisms of normal bone marrow function and development of cancer. Among those affected, the majority develop cancer, most often acute myelogenous leukemia (AML), and 90% develop aplastic anemia (the inability to produce blood cells) by age 40. About 60–75% have congenital defects, commonly short stature, abnormalities of the skin, arms, head, eyes, kidneys, and ears, and developmental disabilities. Around 75% have some form of endocrine problem, with varying degrees of severity. FA is the result of a genetic defect in a cluster of proteins responsible for DNA repair via homologous recombination.Treatment with androgens and hematopoietic (blood cell) growth factors can help bone marrow failure temporarily, but the long-term treatment is bone marrow transplant if a donor is available. Because of the genetic defect in DNA repair, cells from people with FA are sensitive to drugs that treat cancer by DNA crosslinking, such as mitomycin C. The typical age of death was 30 years in 2000.FA occurs in about one per 130,000 births, with a higher frequency in Ashkenazi Jews and Afrikaners in South Africa. The disease is named after the Swiss pediatrician who originally described this disorder, Guido Fanconi. It should not be confused with Fanconi syndrome, a kidney disorder also named after Fanconi.