A variety of bis and tris thiobiureto and dithiobiureto Co(II), Ni(II), Cd(II), Cu(II), Zn(II) metal complexes were synthesized by reacting N,N-dialkylcarbamoyl or N,N-dialkylthiocarbamoyl with potassium thiocyanide and twelve different commercially available amines. These complexes were characterized by spectroanalytical (UV-Vis, FT-IR, 1H-NMR and 13C-NMR) and single crystal X-ray diffraction techniques. To find percentage composition of atoms i.e. C, H and N present in synthesized complexes were also determined by CHN analysis. The obtained data from UV-Visible, FT-IR, 1H NMR, 13C NMR and elemental analysis were compared with the reported values which satisfactorily justified the synthesis of thiobiuret and dithiobiuret metal complexes. The structure of five complexes such as bis(1,1,5,5-tetramethyl-2,4-dithiobiureto)nickel(II) 12, bis(1,1,5,5-tetramethyl-2-thiobiureto)copper (II) 24, bis (1,1,5,5-tetramethyl-2,4-dithiobiureto) cadmium (II) 36, bis[(Z)-3-(3,3-dimethylbutanyol)-1,1-diethyl-2-thiobiureto]nickel (II) 48 and tris[(Z)-3-(3,3-dimethylbutanyol)-1,1-diethyl-2-thiobiureto] cobalt(II) 54 was unambiguously confirmed with single crystal X-ray analysis, establishing that the geometry of Ni(II), Cd(II) complexes (12, 36) is tetrahedral, square planar for Cu(II) and Ni(II) (24, 48) and octahedral geometry for (54) Co(II) complexes. Synthesized complexes were considered to evaluate their conductance and results indicate that they possess differential levels of electrolytic characteristics, which indicates that complexes had positive electrolytic behavior, whereas few complexes showed suppressed electrolytic properties. Regarding the assessment of antibacterial, antifungal, protein kinase inhibition, total antioxidant capacity, reducing power, DPPH radical scavenging, xxi ABTS antioxidant potential and anticancer assay; fourteen synthesized complexes were used for antibacterial and antifungal activity, thirty two complexes were considered for rest of the abovementioned assays. Out of fourteen complexes 8, 12, 13, 14, 27, 32, 38 had significant activities against three bacterial strains i.e. Echerishia coli, Staphylococcus aureus and Pseudomonas aeruginosa due to NCS containing moieties and 2, 3, 4, 12, 14, 27, 38, 47 possess differential levels of inhibition against Aspergilus niger, Flavus solani, Mucor species and Aspergilus flavus microbes. Out of thirty two said complexes on the other hand, 3, 5, 7, 10, 13, 15, 17, 19, 28, 46 and 1-8, 10, 12, 13, 14, 16-19, 22, 28-31, 43, 46 complexes were found as potential agents for protein kinase inhibition and antioxidant activity, respectively. Furthermore, all said synthesized transition metal complexes possessed significant inhibition activity against the cancer cell line. In all, biological findings obtained through the present study indicate that almost all synthesized complexes are promising candidates to combat cancer effect by suppressing oxidative stresses, and as well as anti-microbial activity to control infections. However, further comprehensive animal based studies are warranted to confirm our results to be translated them as drugs/medicines in future.
ڈاکٹر سید محی الدین زور قادری اردو زبان کے مشہور خدمت گذار اور نامور صاحبِ قلم ڈاکٹر سید محی الدین زور قادری کی وفات دنیائے اردو کا بڑا سانحہ ہے، انھوں نے علمی اور عملی دونوں حیثیتوں سے اردو زبان و ادب کی بڑی خدمت کی، وہ دکن کے مولوی عبدالحق اور دکنیات کے خصوصیت کے ساتھ بڑے ماہر تھے، قدیم دکھنی اردو کی بہت سی نادر کتابیں انھوں نے شائع کیں، ان کاسب سے بڑا کارنامہ ادارۂ ادبیاتِ اردو حیدرآباد ہے، اس ادارہ نے اردو زبان و ادب کی جو گوناگوں خدمات انجام دیں، اس کی مثال اردو کے اس کی عمر کے اداروں میں نہیں مل سکتی، اس کی․․․․․․․ حیثیت دکن میں وہی ہے، جو شمالی ہند میں انجمن ترقی اردو ہند کی ہے اور آج اندھراپردیش میں اردو کا وجود اور اس کا وقار اسی ادارے کے دم سے قائم ہے، ڈاکٹر زور کی مستقل تصانیف اور ان کی مرتب اور شائع کردہ کتابوں کی تعداد ایک درجن سے زیادہ ہوگی، وہ حیدرآباد کے ایک خانوادۂ مشائخ سے تعلق رکھتے تھے، اسی نسبت سے اپنے نام کے ساتھ قادری لکھتے تھے، اور اس سلسلہ کو انھوں نے قائم بھی رکھا تھا، چناچہ ان کے بڑے صاحبزادے ان کی خاندانی خانقاہ کے سجادہ نشین ہیں، مگر ان کی علمی و ادبی شہرت نے ان کی اس حیثیت کو اتنا چھپا دیا تھا کہ اس کا علم بھی بہتوں کو نہیں ہے، اﷲ تعالیٰ ان کی مغفرت فرمائے۔ (شاہ معین الدین ندوی، اکتوبر ۱۹۶۲ء)
يهدف هذا البحث إلى جمع الأحاديث الواردة في محبة الله عز وجل من الصحيحين، ودراستها واستنباط الأحكام والفوائد منها، وإثبات صفة المحبة لله تعالى، وأنه سبحانه يحب عباده، ويحبه عباده، وهو مذهب أهل السنة والجماعة. كما أن هذا البحث يبين ما يحبه الله من الأعمال والأقوال والأخلاق التي وردت بها سنة النبي صلى الله عليه وسلم، وقد أوردت فيه الأسباب الموجبة لمحبته سبحانه، وثمرات تلك المحبة. وخلص الباحث إلى أنَّ محبة الله جل وعلا واجبة، وأن لها آثاراً تترتب عليها، ومقتضيات يجب تحقيقها، وأن محبة الله للعبد لها علامات يستدل بها على ذلك.
Hearing loss is a common neurosensory impairment, which has a significant genetic etiology. A hearing loss affects 1 in 1000 newborns and 1 in 300 children by the age of 4 years (Chang 2015). It has been estimated that 1% of almost 30,000 protein coding genes in human are associated with hearing phenotype (Friedman and Griffith 2003). The mechanism of hearing is not fully understood because of the challenges associated with studying inner ear architecture, but nonetheless some of the key genes encoding distinct mechanisms of hearing have been explored by using genetic tools. Recent studies in the field of human genetics have been influential in identifying some of the proteins underlying mechanisms essential for sound transduction, as for example, hair cells electromotility, mechanotransduction, development of inner and outer hair cells, and the molecular composition of the ribbon synapse. Using a genetic approach, this thesis research project explored novel genes involved in non-syndromic and syndromic forms of hearing loss. Participants from 85 families that are segregating moderate to severe degree of hearing loss are included in this study. The affected individuals from 85 different families were initially screened for mutations of GJB2 and HGF. Genetic variants of these two genes are common in the Pakistani population and there is only one protein-coding exon of GJB2 and two common intronic mutations of HGF which are easily sequenced for mutations. I have identified twenty five novel mutations in genes that have been associated with hearing loss and all of the identified novel mutations are predicted to be pathogenic according to multiple in silico tools and have an allele frequency less than 0.005%. Mutations of MYO15A, GJB2 and HGF are the three-major contributors to deafness in this cohort of eighty-five families. In this thesis research project, I have successfully utilized some of the latest techniques in genetics that includes Whole Exome Sequencing (WES), genome wide SNP genotyping, and Whole Genome Sequencing (WGS) and was able to identify novel genes involved in syndromic and non-syndromic forms of deafness. In family PKDF1400, I completed genome wide SNP genotyping of affected and unaffected individuals. Genotyping data revealed a significant linkage score on chromosome 19p13.2 that encompasses DFNB68 locus. Individuals from PKDF1400 were then subjected to WES and I identified a missense pathogenic variant of S1PR2 (p.Tyr140Cys). Sanger sequencing of the single nucleotide variant revealed co segregation with the phenotype in PKDF1400. This thesis project has contributed data in identifying a novel gene underlying DFNB68 form of deafness (Santos-Cortez et al. 2016). I also identified a variant of SGO2 that is necessary for fertility in a Perrault syndrome proband of family PKDF063, which was ascertained from Pakistan. Whole exome sequencing of affected and unaffected members of PKDF063 revealed a truncating mutation of SGO2 p.(Glu485Lysfs*5) associated with the proband’s infertility phenotype. This is the first report of an association of SGO2 with human infertility (Faridi et al. 2017). I was successful in identifying a rare truncating mutation in family PKDF461 using Whole genome sequencing. PKDF461 was ascertained as a family segregating non syndromic hearing loss. The family has significant linkage of deafness to the DFNB8/10 interval which was further narrowed after analyzing WGS data that revealed a novel nonsense mutation of KCNE1 (p.Tyr46*). Mutations of KCNE1 are associated with Jervell and Lange Nielson syndrome (JLNS2) but this is the first truncating mutation of this gene.Overall, this thesis research project has identified novel gene for human hearing and fertility and has expanded the genotype-phenotype spectrum associated with Perrault syndrome and Jervell and Lange Nielson syndrome. This study has contributed twenty five novel genetic variants in several different genes that are critical for normal auditory function. Overall, this research project utilized cutting-edge genomic technologies that have revealed molecular genetic explanations for hereditary hearing loss in human families and was successful in identifying novel genes for non-syndromic and syndromic forms of hearing loss.