حد الزاني البكر و المحصن

Islam is a complete code of life and it provides complete guidance in every field of life. Islamic law provides protection to the human wisdom, race and respect. Spiritual purity, sacred heart and environmental cleanliness, is one of the important persistence of Islamic sharia. Every act which leads us towards ignorance, contradiction, ambiguity and vulgarity is prohibiting in human societies. Zina has destroyed the spiritual values of individuals, families, societies and even nations. This ruthless deed is not only prohibited and sentenced in Islam, but also rather detested by other heavenly religions as well. Without discrimination of any religion, many scholars considered this hated act as the source of unrest and anarchy. Physically, ethically, medically, socially and even religiously zina has infinite hindrances in the society. Islam has provided various teachings and precautions to shun from this major sin for the protection of greatness and superiority of humanity. One of the important teachings is punishment for committing this sin, which is known as “Hadd” in Islamic sharia. In the current book, the punishments of married and unmarried (Fornicator) zani have been described in the light of Sunnah and Quran. The important purpose of Qisas and Hadd is the correction of societies, protection of life, respect and wealth, not the humiliation of people. To punish the criminals is the source of rectification for others.

Genetic Mapping and Mutation Analysis of Genes Causing Disorders of Human Ectodermal Appendages

The study, presented in the thesis, is an effort to explore genetic basis of disorders of ectodermal appendages in different ethnic populations living across Pakistan. Hereditary hypotrichosis and ectodermal dysplasias are large, complex and heterogeneous groups of heritable conditions characterized by congenital abnormalities of ectodermal appendages. They can broadly be characterized into two groups depending upon the absence (isolated) or presence (syndromic) of associated defects in other organ/organ systems. Discovery of genes responsible for these disorders is the key source of insight into the molecular mechanisms of development and differentiation of ectodermal appendages. Focus of the present study was to identify and characterize genes causing hereditary disorders of ectodermal appendages in fifteen families (A-O) of Pakistani origin. Eleven of these families (A-K) were segregating various types of hair loss disorders and four families (L-O) ectodermal dysplasias. Combination of various techniques including microsatellite and SNP genotyping, Sanger sequencing and exome sequence analysis assisted in establishing linkage and identifying disease causing variants in the families. Four families (A, B, C, D) with non-syndromic hair loss failed to show linkage to the known genes. Subsequently, three of them were subjected to whole-genome SNP genotyping. Human genome scan mapped a novel disease locus of 10.85 Mb on chromosome 2q31.1–q32.2 in family A. Sequencing of the three selected putative candidate genes (ITGA6, PRKRA, ATF2), mapped in the linkage interval, did not reveal any functional variant in the family. Family B showed linkage to chromosome 6p25.1–p23, and subsequently a novel variant (c.1493C>T; p.Pro498Leu) in the DSP gene was identified upon sequencing. Whole-genome SNP genotyping coupled with whole exome sequencing identified two compound heterozygous deletions, a novel (c.278_278delA; p.Lys93Argfs*9) and a previously reported (c.659_660delTA; p.Ile220Argfs*25), in the LIPH gene in family D. Genetic Mapping and Mutation Analysis of Genes Causing Disorders of Human Ectodermal Appendages xixAbstract Six families (E, F, G, H, I, J) with non-syndromic hair loss showed linkage to previously reported genes (LIPH, LPAR6, HR) involved in causing hypotrichosis. Linkage in four of these families (E, F, G, H) was established to the LIPH gene on chromosome 3q26.33–q27.3. Sequence analysis of the LIPH revealed a previously described deletion (c.659-660delTA; p.Ile220Argfs*25) in three families (F, G, H). However, sequence analysis failed to detect variant in the LIPH gene in family E. Haplotype analysis showed linkage of the family I to the LPAR6 gene on chromosome 13q14.11–q21.32. Sequence analysis of the gene revealed a previously described variant (c.562A>T; p.Ile188Phe) in the family. In the family J, linkage was established to the HR gene on chromosome 8p21.3. Sequencing of the gene revealed a previously reported variant (c.2070C>A; p.Cys690*). In the family K, segregating novel features associated with hair loss, exome sequence analysis led to the identification of a novel rare variant (c.898G>A; p.Glu300Lys) in ITGB6 gene that co-segregated with the phenotype in the family. Four families (L-O) showed features of different forms of ectodermal dysplasias. The family L showed features of pure hair and nail ectodermal dysplasia (PHNED). Haplotype analysis mapped the family to the previously reported locus on chromosome 12p13.11–q21.1. Three genes (KRT85, HOXC13, KRT74), known to cause PHNED lie in this region, were screened but found to be negative for any potential sequence variant. Haplotype analysis established linkage to the previously proposed locus on chromosome 4q32.3–q34.3 in family M segregating isolated form of congenital nail clubbing (ICNC). HPGD, a cause of ICNC, lies in this region, was sequenced but found to be negative for any potential variant. Genome-wide homozygosity mapping complimented with whole exome sequencing identified a previously reported variant (c.5314C>T; p.Arg1772Trp) in COL7A1 segregating autosomal recessive form of dystrophic epidermolysis bullosa (RDEB) in the family N. In family O, segregating variegate porphyria (VP), exome sequence analysis led to the identification of a previously described sequence variant (c.502C>T; p.Arg168Cys) in the PPOX gene that co-segregated with the disease.