8 results on '"Farah Umar"'
Search Results
2. Integrated and Site-Specific Fertilizer Application Role in Rice-Wheat Cropping System
- Author
-
Umair Riaz, Abdul Ghaffar, Muhammad Akram Qazi, Naveed Iqbal Khan, Zubaida Hamid, Khalid Mehmood Mughal, Niaz Ahmed, Ashfaq Ahmad Rahi, Imtiaz Ahmad Warraich, Mahreen Khalid, Saima Nazar, and Farah Umar
- Subjects
Rice wheat cropping ,Agronomy ,engineering ,Environmental Chemistry ,Rice wheat ,Fertilizer ,Biology ,engineering.material ,General Environmental Science - Published
- 2021
3. IDENTIFIKASI BAKTERI ASAM LAKTAT ASAL USUS BANDENG Chanos chanos DENGAN GEN PENGKODE 16S rRNA
- Author
-
Setianingtyas, Farah Umar
- Subjects
Bandeng Chanos chanos, Bakteri asam laktat, 16S rRNA, Lactobacillus plantarum, Enterococcus faecalis - Abstract
Telah dilakukan penelitian Identifikasi Bakteri Asam Laktat Asal Usus Bandeng Chanos chanos dengan Gen Pengkode 16S rRNA. Penelitian ini bertujuan untuk mengidentifikasi bakteri asam laktat asal usus ikan Bandeng Chanos chanos secara molekuler dengan gen 16S rRNA. Kelima isolat bakteri asam laktat diekstraksi menggunakan Geneaid PrestoTM Mini gDNA Bacteria Kit. Hasil ekstraksi DNA diamplifikasi dengan metode PCR menggunakan primer universal gen 16S rRNA yaitu primer Forward 63F (5???-CAGGCCTAACACATGCAAGTC-3???) dan primer Reserve 1387R (5???-GGGCGGWGTGTACAAGGC-3???), hasil amplifikasi divisualisasikan pada elektroforesis dan dihasilkan pita DNA yang sejajar dengan marker 1300 bp. Hasil PCR disekuensing kemudian sekuens yang diperoleh di-BLAST untuk mengkonfirmasi spesies. Hasil penelitian menunjukkan 2 isolat (IPB6 dan IPB9) teridentifikasi sebagai bakteri Lactobacillus plantarum strain WCFS1. Sedangkan 3 isolat (IPB3, IPB7, dan IPB9) teridentifikasi sebagai bakteri Enterococcus faecalis strain NBRC 100480. Berdasarkan rekonstruksi pohon filogeni dengan Neighbor-Joining bootstrap 1000x (MEGA 6.60) didapatkan 2 klad (kelompok) besar yaitu klad pertama Enterococcus faecalis dan klad kedua lactobacillus plantarum.
- Published
- 2015
4. Pathogenic antibodies in women with obstetric features of antiphospholipid syndrome who have negative test results for lupus anticoagulant and anticardiolipin antibodies
- Author
-
Farah Umar, Robert M. Silver, Silvia S. Pierangeli, Samuel S. Edwin, D. Ware Branch, James R. Scott, and E. Nigel Harris
- Subjects
Abortion, Habitual ,Mice, Inbred Strains ,Immunoglobulin G ,Mice ,Pregnancy ,immune system diseases ,Antiphospholipid syndrome ,Immunopathology ,medicine ,Animals ,Humans ,skin and connective tissue diseases ,Fetal Death ,Autoimmune disease ,Lupus anticoagulant ,biology ,business.industry ,Immunization, Passive ,Obstetrics and Gynecology ,Antiphospholipid Syndrome ,medicine.disease ,Immunization ,Antibodies, Anticardiolipin ,Lupus Coagulation Inhibitor ,Immunology ,Antibodies, Antiphospholipid ,biology.protein ,Pregnancy, Animal ,Female ,Antibody ,business - Abstract
OBJECTIVE: Our goal was to determine whether women with clinical features of antiphospholipid syndrome but negative test results for lupus anticoagulant and anticardiolipin antibodies have pathogenic antibodies not identified by currently used methods. STUDY DESIGN: Sera were obtained from women with clinical features associated with antiphospholipid antibodies who had negative test results for lupus anticoagulant and anticardiolipin antibodies (antiphospholipid syndrome–like). We studied (1) the effect of passive immunization with their purified immunoglobulin G fraction on murine pregnancy ( n = 35) and (2) the presence of antiphospholipid antibodies other than lupus anticoagulant or anticardiolipin antibodies ( n = 39). Sera were also retested for anticardiolipin antibodies and lupus anticoagulant. RESULTS: Fetal loss occurred in 235 of 1088 (22%) pups in 137 mice immunized with immunoglobulin G fraction from antiphospholipid syndrome–like women compared with 23 of 402 (6%) pups in 53 control mice. Immunoglobulin G from 11 study patients resulted in the loss of at least one third of the exposed pups. Five women had positive levels of antiphosphatidylserine antibodies (>99th percentile). All levels were low positive, and three women also had low-positive levels of anticardiolipin antibodies on repeat testing. Five of the 11 (45%) women whose immunoglobulin G fractions caused at least 33% fetal loss also had positive test results for antiphospholipid antibodies. CONCLUSIONS: A subset of women with clinical disorders suspicious for antiphospholipid syndrome but who had negative test results for lupus anticoagulant and anticardiolipin antibodies by current methods have serum immunoglobulin G that is pathogenic to murine pregnancy. Testing for pathogenic immunoglobulin G may provide additional means to identify women with an as yet uncharacterized immune condition. The clinical relevance of low levels of antiphospholipid antibodies in these women remains unproved. (Am J Obstet Gynecol 1997;176:628-33.)
- Published
- 1997
5. Stuttering as a phenotype for behavioral genetics research
- Author
-
Farah Umar, Charles David Mellon, and Marvin L. Hanson
- Subjects
Adult ,Male ,Behavioral phenotypes ,Stuttering ,Genetics, Behavioral ,Biology ,Age Distribution ,Central Nervous System Diseases ,Communication disorder ,Prevalence ,medicine ,Humans ,Language disorder ,Sex Distribution ,Child ,Genetics (clinical) ,Behavioural genetics ,Genetics ,Phenocopy ,Research ,medicine.disease ,Phenotype ,nervous system diseases ,Child, Preschool ,Etiology ,Female ,medicine.symptom - Abstract
Stuttering is a broad behavioral phenotype with an adult prevalence of 0.7-1.0%. Family, twin, and segregation studies all indicate that stuttering has a large genetic component to its etiology. The relatively simple phenotype, the early onset, and the apparent rarity of phenocopies of adult stuttering all make stuttering a promising model for the study of the genetics of broad behavioral phenotypes.
- Published
- 1993
6. Bacterial lipopolysaccharide-mediated murine fetal death: the role of interleukin-1
- Author
-
Farah Umar, Murray D. Mitchell, Donald J. Dudley, Robert M. Silver, Samuel S. Edwin, and D. Ware Branch
- Subjects
Lipopolysaccharides ,medicine.medical_specialty ,Lipopolysaccharide ,medicine.medical_treatment ,Indomethacin ,Prostaglandin ,Mice, Inbred Strains ,Chorioamnionitis ,Antibodies ,Dinoprostone ,chemistry.chemical_compound ,Mice ,Pregnancy ,Internal medicine ,medicine ,Animals ,Fetal Death ,Fetus ,Mice, Inbred C3H ,business.industry ,Decidua ,Obstetrics and Gynecology ,Interleukin ,Receptors, Interleukin-1 ,medicine.disease ,Endocrinology ,medicine.anatomical_structure ,chemistry ,Tumor necrosis factor alpha ,Female ,business ,Prostaglandin E ,Interleukin-1 - Abstract
OBJECTIVE: Our purpose was to determine whether interleukin-1 is an important mediator of lipopolysaccharide-induced fetal death and, if so, whether interleukin-1 causes fetal death by inducing prostanoid formation in gestational tissues. STUDY DESIGN: Pregnant C3H/HeN mice were administered lipopolysaccharide, interleukin-1α, interleukin-β, or vehicle on days 11 to 13 of pregnancy. Mice were killed 72 hours later and the fetal status was determined. Some mice were pretreated with anti-interleukin-1-receptor antibodies or indomethacin. Decidual explants were established from treated mice, and supernatants were assayed for interleukin-1β and prostaglandin E 2 . RESULTS: Decidua taken from lipopolysaccharide-treated mice produced significantly increased amounts of interleukin-1β, and pretreatment with anti-interleukin-1-receptor antibodies reduced the proportion of fetal deaths after lipopolysaccharide administration from 100% to 33%. The administration of interleukin-1α caused fetal death in a dose-dependent fashion, and decidua taken from interleukin-1–treated mice produced significantly increased amounts of prostaglandin E 2 . However, pretreatment with doses of indomethacin that abrogated decidual prostaglandin E 2 production did not reduce the proportion of fetal death after interleukin-1α administration. CONCLUSIONS: Interleukin-1 is an important mediator of lipopolysaccharide-induced fetal death and causes fetal death by prostaglandin-independent effects.(Am J Obstet Gynecol 1997;176:544-9.)
- Published
- 1997
7. Schizophrenia and GABAA receptor subunit genes
- Author
-
Farah Umar, Mark Hoff, Robert Freedman, John Holik, Mark E.S. Bailey, Hilary Coon, William Byerley, Marina Myles-Worsley, Paul H. Wender, M. G. Darlison, K. J. Johnson, Merilyne Waldo, Frederick W. Reimherr, A. A. Hicks, and B. P. Riley
- Subjects
Genetics ,Beta-3 adrenergic receptor ,GABAA receptor ,Alpha (ethology) ,Genes, Recessive ,Minisatellite Repeats ,Biology ,Receptors, GABA-A ,Gamma-aminobutyric acid receptor subunit alpha-1 ,GABAA-rho receptor ,Nuclear Family ,Pedigree ,Beta-1 adrenergic receptor ,Psychiatry and Mental health ,Genetic linkage ,Schizophrenia ,Humans ,Lod Score ,Gene ,Biological Psychiatry ,Genetics (clinical) ,Genes, Dominant - Abstract
Alterations in gamma-aminobutyric acid (GABA) neurotransmission have been indirectly implicated in the pathogenesis of schizophrenia. Using nine multiplex pedigrees, we tested for linkage between schizophrenia and simple sequence repeat polymorphisms for the GABAA receptor alpha 1, alpha 2, alpha 4, alpha 5, alpha 6, beta 1 and beta 3 subunit genes. Evidence of linkage was not found when assuming either autosomal dominant or autosomal recessive inheritance. The non-parametric sib pair test also did not reveal significant evidence of deviation from expected segregation ratios.
- Published
- 1995
8. Search for mutations in the beta 1 GABAA receptor subunit gene in patients with schizophrenia
- Author
-
William Byerley, Janet L. Sobell, Margaret Robertson, Paul H. Wender, Steve S. Sommer, James M. Sikela, Mark Hoff, Gail Shields, Kevin Vest, Lynn E. DeLisi, Merilyne Waldo, John Holik, Sherry Leonard, Elliot S. Gershon, Farah Umar, Frederick W. Reimherr, Anthony Polloi, Robert Freedman, Paul W. Dale, Hilary Coon, Leonard L. Heston, and Marina Myles-Worsley
- Subjects
Male ,Psychosis ,medicine.medical_specialty ,Adolescent ,DNA Mutational Analysis ,Molecular Sequence Data ,Biology ,Gene mutation ,Polymerase Chain Reaction ,Exon ,Dopamine receptor D3 ,Polymorphism (computer science) ,Pregnancy ,medicine ,Humans ,Point Mutation ,Amino Acid Sequence ,Genetics (clinical) ,Alleles ,Aged ,DNA Primers ,Genetics ,Polymorphism, Genetic ,Base Sequence ,Single-strand conformation polymorphism ,Exons ,Middle Aged ,medicine.disease ,Receptors, GABA-A ,Pedigree ,Schizophrenia ,Medical genetics ,Nucleic Acid Conformation ,Female - Abstract
As alterations in GABAergic neurotransmission have been indirectly implicated in the pathogenetics of schizophrenia, GABAA receptor subunit genes are plausible candidate genes for the illness. We undertook a search for sequence variations in the coding region of beta 1 subunit gene by designing intron-based primers to amplify its 9 exons. Using single strand conformation polymorphism (SSCP) analysis, we found an exon 9 variant present in 3 of 86 unrelated schizophrenic cases derived from families having at least 2 first-degree relatives with schizophrenia. Direct sequencing of the SSCP variant revealed a C--G nucleotide transversion at codon 396 predicting a histidine to glutamine substitution in the beta 1 peptide. The predicted amino acid substitution occurs at a highly conserved site, 9 residues from a cAMP-dependent serine phosphorylation consensus sequence. All known GABAA beta 1 subunit genes including human, bovine, and rat, code for histidine at position 396. Although the variant cosegregated with disease in a family with 2 affected sibs, it was only transmitted to 2 of 3 affected sibs in a multiplex family. The variant was not found in an additional sample comprising 155 unrelated schizophrenics and the sequence variant was present at a low frequency (approximately 1.1%) in control groups. Although these results indicate that the sequence variant is likely to be a natural polymorphism, it is possible that the variant may be a predisposing allele in rare instances. It is also possible that the variant may change the function or regulation of the GABAA receptor complex and it may be of pharmacogenetic relevance.
- Published
- 1994
Catalog
Discovery Service for Jio Institute Digital Library
For full access to our library's resources, please sign in.