scispace - formally typeset
Search or ask a question
Author

B. I. Sahai Srivastava

Bio: B. I. Sahai Srivastava is an academic researcher from Roswell Park Cancer Institute. The author has contributed to research in topics: Terminal deoxynucleotidyl transferase & DNA polymerase. The author has an hindex of 21, co-authored 65 publications receiving 1304 citations. Previous affiliations of B. I. Sahai Srivastava include University at Buffalo & New York State Department of Health.


Papers
More filters
Journal ArticleDOI
TL;DR: It is shown that the female genital tract immunologically does not reject spermatooa nor the preimplantation and nidating embryo, and the number of cells in the genital tract increases with age and disease progression.
Abstract: PROBLEM: How is it possible that the female genital tract immunologically does not reject spermatooa nor the preimplantation and nidating embryo? METHODS: Four fluids of the human reproductive tract, i.e., human oviductal fluid (hOF), follicular fluid (FF), amniotic fluid (AF), and seminal plasma (SP) were investigated by specific ELISA for 18 cytokines. The concentrations, presence or absence of these compounds were evaluated for their possible role in the immunology of the reproductive process. RESULTS: Stem cell factor and IL-11 were detected in all reproductive tract fluids examined whereas large amounts of IL-1β and IL-1RA was found in AF and hOF. Follicular fluid revealed IL-2. HOF contained IL 2, IL-6, IL-8, TNF-α, MIP-1α, IFN-γ, and high levels of IL-1β, IL-10, IL-1RA, and sIL-2R. Amniotic fluid contained sIL-2R, IL-8, IL-1β, IL-1RA, IL-6, TNF-α, and MIP-1α. No IL-12 or IL-13 was detected in hOF, follicular fluid, or amniotic fluid. Almost no free TGF-β1 or TGF-β2 was found in any reproductive tract fluid except seminal plasma. Seminal plasma contained large quantities of free TGF-β1 (9,220 ± 3,635 pg/mL) in addition to large quantities of latent TGF-β2 (2,933 ± 2,169 pg/mL) and TGF-β, (71,000 ± 3,240 pg/mL). Furthermore, considerable concentrations of IL-8 (1900 ± 374 pg/mL) and sIL-2R (350 μ/mL) exist in seminal plasma. CONCLUSIONS: HOF contains a high level of IL-10 (588 ± 304 pg/mL), a powerful immune suppressor which probably plays a role in regulating immune responses in the fallopian tube and possibly in the endometrial cavity. Our observations suggest that seminal plasma with its huge content of TGFβ provides immune protection for sperm. Unfortunately, such high concentrations of TGFβ may also inhibit an immune defense in any organ in which semen is deposited.

124 citations

Journal ArticleDOI
TL;DR: A terminal deoxynucleotidyl transferase having a sedimentation coefficient of 3–4S has been found associated with the chromatin from a cell line (Molt-4) derived from the peripheral blood of a patient with acute lymphoblastic leukemia.

92 citations

Journal ArticleDOI
TL;DR: The results suggest that aATP and aCTP inhibit terminal deoxynucleotidyl transferase by competing with any substrate for binding to the enzyme and DNA polymerases α and β by specifically competing with their analogs (dATP or dCTP) forbinding to these enzymes.
Abstract: Both 9-β-D-arabinofuranosyladenine 5′-triphosphate (aATP) and 1-β-D-arabinofuranosylcytosine 5′-triphosphate (aCTP) inhibit terminal deoxynucleotidyl transferase and DNA polymerases α and β but not DNA polymerase γ from human cells. Inhibition of terminal deoxynucleotidyl transferase by both compounds is competitive with respect to either dGTP, dCTP, dATP, or dTTP and inhibition of DNA polymerases α and β is competitive with respect to dATP (for aATP) and dCTP (for aCTP). The inhibition constants for aATP for each enzyme are lower than the inhibition constants for aCTP implying that aATP has a stronger affinity for each enzyme than aCTP. In addition, the inhibition constants for aATP for each enzyme are about equal, suggesting that the drug binds to each enzyme with about the same affinity. The same is true for aCTP. Both compounds are non-competitive inhibitors of terminal deoxynucleotidyl transferase with respect to initiator [(dA)12–18], uncompetitive inhibitors of DNA polymerases α and β with respect to template/primer (activated DNA), and non-competitive inhibitors of DNA polymerases α and β with respect to a non-analogous substrate (dTTP). Inhibition of all three enzymes was reversed by simple dilution but not by additional enzyme, template/primer, initiator, or divalent cation. These results suggest that aATP and aCTP inhibit terminal deoxynucleotidyl transferase by competing with any substrate (dGTP, dCTP, dATP, or dTTP) for binding to the enzyme and DNA polymerases α and β by specifically competing with their analogs (dATP or dCTP) for binding to these enzymes.

70 citations

Book ChapterDOI
TL;DR: It is important to note that cytokinins are also transported through the xylem in intact plants, as cytokinin-like compounds have been detected in the sap of several plants.
Abstract: Publisher Summary This chapter focuses on the group of plant hormones called cytokinins, which are defined as compounds that induce cell division in plant cells in cooperation with an auxin. Gibberellins move in plants in a nonpolar fashion, whereas the cytokinins have been reported to move like auxins in a basipetal polar fashion. Cytokinins are extensively metabolized by plant tissues should be kept in mind in studying their transport. In connection with the movement of cytokinins in plants, it is important to note that cytokinins are also transported through the xylem in intact plants, as cytokinin-like compounds have been detected in the sap of several plants. Adenine derivatives with substituents at positions 2, 7, and 9 are inactive, whereas 1-benzyladenine and 1-(3,3-dimethylallyl) adenine showed cytokinin activity, and 3-(3,3-dimethylallyl)adenine (triacanthine), which occurs naturally in plants, showed cytokinin activity only after its conversion, through autoclaving, to the 6-isomer. The chapter discusses the biological effects of cytokinins, metabolism and intracelldar localization of cytokinins in plants, mechanism of action of cytokinins, and metabolic effects of cytokinins.

44 citations


Cited by
More filters
Journal ArticleDOI
TL;DR: Antibodies against the antigen in MT-1 cells were found in all 44 patients with ATL examined and in 32 of 40 patients with malignant T-cell lymphomas (most of them had diseases similar to ATL except that leukemic cells were not found in the peripheral blood).
Abstract: Indirect immunofluorescence of certain human sera demonstrated an antigen(s) in the cytoplasm of 1--5% of the cells of a T-cell line, MT-1, from a patient with adult T-cell leukemia (ATL), which is endemic in southwestern Japan. The antigen was not detected in other human lymphoid cell lines, including six T-cell lines, seven B-cell lines, and four non-T non-B cell lines. The antigen did not show cross antigenicity with that of herpesviruses, including Epstein--Barr virus, herpes simplex virus, cytomegalovirus, varicella-zoster virus, herpesvirus saimiri, and Marek disease virus. The proportion of antigen-bearing cells was increased by a factor of approximately 5 on culture in the presence of 5-iodo-2'-deoxyuridine. Antibodies against the antigen in MT-1 cells were found in all 44 patients with ATL examined and in 32 of 40 patients with malignant T-cell lymphomas (most of them had diseases similar to ATL except that leukemic cells were not found in the peripheral blood). The antibodies were also detected in 26% of the healthy adults examined from ATL-endemic areas but in only a few of those examined from ATL-non-endemic areas. On electron microscopy, extracellular type C virus particles were detected in pelleted MT-1 cells cultured in the presence of 5-iodo-2'-deoxyuridine.

2,102 citations

Journal ArticleDOI
TL;DR: This work states that the "SOS" Hypothesis, the Regulatory Role of DNA Damage in E. coli, and the Mechanism of SOS Repair in Bacteria and other UV-INDUCIBLE FUNCTIONS, and Regulations of SOS REPAIR, are valid hypotheses for the regulation of SOS functions.
Abstract: INTRODUCTION .............................................................. 869 Enzymatic Repair of UV Damage in E. coli ......... .......................... 869 Error-Proof and Error-Prone Pathways of DNA Repair ....... ................. 871 The \"SOS\" Hypothesis: the Regulatory Role of DNA Damage ...... ............ 874 EVIDENCE FOR THE INDUCIBILITY OF ERROR-PRONE REPAIR (\"SOS REPAIR\") ACTIVITY ..................................................... 875 SOS Repair of Bacteriophage DNA ............ ............................... 875 SOS Repair of Bacterial DNA ................ ................................ 876 Evidence from studies of repair-deficient mutants ....... .................... 876 Evidence from studies of postreplication repair ........ ...................... 879 MANIFESTATIONS OF SOS REPAIR AND THEIR SIGNIFICANCE ..... ...... 879 Mutation Frequency Response to Increasing Fluence of UV Radiation ..... ..... 879 The UV Lesion Responsible for Induction of SOS Functions.................... 880 Kinetics of Induction and Decay of SOS Repair Activity ....... ................ 882 Time of Action of SOS Repair in UV Mutagenesis ...... ........................ 882 Cryptic Premutational Lesions Susceptible to SOS Repair ...................... 884 Mutator Effect of SOS Repair on Undamaged DNA ....... ..................... 885 PLASMIDS AND SOS REPAIR ................................................ 886 MECHANISM OF SOS REPAIR ............................................... 886 Mechanism of SOS Repair in Bacteriophage ......... .......................... 886 Mechanism of SOS Repair in Bacteria ........... ............................. 887 IMPLICATIONS OF SOS REPAIR FOR CARCINOGENESIS ................... 888 REGULATION OF SOS REPAIR AND OTHER UV-INDUCIBLE FUNCTIONS . 889 PROTEASES AND THE EXPRESSION OF SOS FUNCTIONS .................. 894 CONCLUSIONS ............................................................... 895 APPENDIX................................................................... 896 LITERATURE CITED ......................................................... 898

1,365 citations

Journal ArticleDOI
TL;DR: It has been postulated that when plants are stressed by certain changes in patterns of weather they become a better source of food for invertebrate herbivores because this stress causes an increase in the amount of nitrogen available in their tissues for young herbivore feeding on them.
Abstract: It has previously been postulated that when plants are stressed by certain changes in patterns of weather they become a better source of food for invertebrate herbivores because this stress causes an increase in the amount of nitrogen available in their tissues for young herbivores feeding on them. And this may cause outbreaks of such phytophagous invertebrates. Evidence is now presented that a similar physiological mechanism appears to operate when a wide variety of apparently unrelated environmental factors impinge on plants or parts of plants in such a way as to perturb their metabolism. A broken branch, lightning strike, fire, nutrient deficiencies or an otherwise adverse site; all may have this effect. With the advent of modern man the available agencies increase and diversify to include pesticides, irradiation and air pollutants. One common metabolic response by plants to all such agents impinging on them seems to be equivalent to that found in senescing plant tissues — the breakdown and mobilization of nitrogen in soluble form away from the senescing/stressed tissues. Young herbivores which chance to feed on such stressed/senescing tissues have a greater and more readily available supply of nitrogen in their food than they would have had if feeding on unstressed plants. As a result many more of them survive, and there is an increase in abundance of their kind. Such increases may be quite localised and short-lived or more widespread and persistent, depending on the extent and duration of the stress experienced by the plants. And in the face of this improved nutrition and survival of the very young, predators and parasites seem to have only a minor influence on subsequent changes in abundance of their herbivorous prey. Another effect of increased mobilization of nitrogen in stressed plants is an increase in the quantity of the seed that they set. This has led to the conclusion that increased abundance of some species of birds at such times is due to a greater supply of seeds as winter food for recent fledglings. But it may be that the increased abundance is due to the synchronous increase in phytophagous insects providing a richer source of protein food for laying hens and growing nestlings.

1,013 citations

Journal ArticleDOI
TL;DR: A classification of the histiocytic disorders that primarily affect children is presented in this article, where guidelines for distinguishing the exceedingly rare malignant diseases of histiocytes from large cell lymphomas through the use of a battery of special studies are provided.
Abstract: Pathologists and pediatric hematologist/ oncologists of the World Health Organization's Committee on Histiocytic/Reticulum Cell Proliferations and the Reclassification Working Group of the Histiocyte Society present a classification of the histiocytic disorders that primarily affect children. Nosology, based on the lineage of lesional cells and biological behavior, is related to the ontogeny of histiocytes (macrophages and dendritic cells of the immune system). Dendritic cell-related disorders of varied biological behavior are dominated by Langerhans cell histiocytosis, but separate secondary proliferations of dendritic cells must be differentiated. Juvenile xanthogranuloma represents a disorder of dermal dendrocytes, another dendritic cell of skin. The hemophagocytic syndromes are the most common of the macrophage-related disorders of varied biological behavior. Guidelines for distinguishing the exceedingly rare malignant diseases of histiocytes from large cell lymphomas through the use of a battery of special studies are provided.

751 citations

Journal ArticleDOI
TL;DR: Renaturation kinetics of labeled Agrobacterium tumefaciens DNA are not influenced by addition of 10(4)-fold excess of crown gall tumor DNA, and PS8 bacteriophage DNA is not detected in crownGall tumor DNA under conditions that allow detection of 0.0007-0.001% added phage DNA.
Abstract: Renaturation kinetics of labeled Agrobacterium tumefaciens DNA are not influenced by addition of 10(4)-fold excess of crown gall tumor DNA. Reconstruction experiments demonstrated that 0.01% added bacterial DNA produces a detectable increase in rate of renaturation of labeled DNA. Crown gall tumor DNA therefore cannot contain as much as 0.01% A. tumefaciens DNA (one entire bacterial genome per three diploid tumor cells). By the same technique, PS8 bacteriophage DNA is not detected in crown gall tumor DNA under conditions that allow detection of 0.0007-0.001% added phage DNA. Crown gall tumor DNA cannot contain as much as one entire phage genome per diploid tumor cell. The presence of a small fraction of either genome (less than 5%), even if present as multiple copies, would escape detection by this method.

672 citations