Cutaneous toxicity of sodium lauryl sulphate, nickel, and their combination in guinea pigs: biochemical and histopathological observations.
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Animals↗
Biomedical subjects
S Narang
Publications and source records attributed to S Narang.
Dermal toxicity of paraphenylenediamine.
The guinea pigs were dermally exposed to paraphenylenediamine (PPD) and in presence of an oxidising agent hydrogen peroxide for 15 and 30 d to assess their effects on some enzymes, lipid peroxidation and histamine contents in the skin. The activities of acid and alkaline phosphatases, beta-glucuronidase, gamma glutamyl transpeptidase, histidase and tyrosinase were enhanced after application of either PPD or PPD plus hydrogen peroxide. The lipid peroxidation and histamine contents also showed marked elevation following exposure to the chemicals.
Acid Phosphatase↗
Dermal exposure of hexachlorophene to guinea pigs.
The skins of guinea pigs were exposed to 50 mg/kg hexachlorophene (HCP) for 7, 15 or 30 days. The activities of skin marker enzymes (beta-glucuronidase, histidase, tyrosinase) increased, but glutathione decreased. Lipid peroxidation and histamine contents increased during different time intervals. The histopathological changes showed damage to epidermis and dermis. Depending on the duration of exposure, HCP produces biochemical and histopathological damage to skin.
Animals↗
Biochemical and histopathological changes following dermal exposure to paraphenylene diamine in guinea pigs.
The guinea pigs were dermally exposed to paraphenylene diamine (PPD) at a dose level of 0.1 ml day-1 of a 1.0% (w/v) solution of PPD for 1, 3, 5 and 7 days. The absorption of PPD and its effects on lipid peroxidation, glutathione, histamine and several enzymes were assessed in skin and serum. Histopathological changes in liver, kidney and skin were examined also. The findings of the study indicated that PPD exposure resulted in significantly increased levels of lipid peroxidation and histamine contents in skin. The activity of enzymes increased significantly in skin and serum. PPD exposure also showed degenerative changes in liver and hyperkeratosis together with infiltration of cells in the dermis. Biochemical defects and histopathological changes in skin and serum correlated with the duration of exposure.
Administration, Topical↗
B lymphocytic lymphoma (large cell) of possible splenic marginal zone origin presenting with prominent splenomegaly and unusual cordal red pulp distribution.
Two cases of large cell lymphoma, B-cell type, primarily involving the red pulp of the spleen rather than the white pulp are described. A number of unusual features suggest that this may be a lymphoma originating from a distinct splenic B-cell lymphocyte whose origin may be the marginal zone of the spleen or the splenic cords. The patients presented with splenomegaly, cytopenias, and no peripheral lymphadenopathy. The gross appearance of the spleens was beefy red without tumor nodules. The tumor cells were primarily in the splenic cords and surrounding residual normal white pulp. There was a minimal hemic phase. The tumor cells had abundant cytoplasm, surface IgM, IgD, kappa, and FC receptors, tartrate-resistant acid phosphatase, but no alkaline phosphatase or interleukin-2 receptors. They had a similar DNA aneuploidy. The most unusual feature was that tumor cells in both cases had phagocytic properties. These lymphomas may be clinically more indolent than their follicular center counterparts.
Adult↗
Central nervous system involvement in a patient with chronic lymphocytic leukemia and non-Hodgkin's lymphoma (Richter's syndrome), with concordant cell surface immunoglobulin and immunophenotypic markers.
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Adult↗
Crystal structure of T4-lysozyme generated from synthetic coding DNA expressed in Escherichia coli.
The polypeptide produced by expressing a chemically synthesized gene coding for the amino-acid sequence of T4-lysozyme has been crystallized and subjected to X-ray diffraction. The crystal structure has been refined to a standard R-factor of 0.191 for data between 8 and 2 A resolution. The refined model is essentially the same as the well-known structure of wild-type T4-lysozyme determined previously by Matthews et al. (1987). Some small changes in the C-terminal region, which is important in maintaining the folded structure, have been noted. In addition to confirming that the synthetic gene product is very close to the wild type, this structure provides a benchmark for protein engineering experiments on the folding and the catalytic activity of this molecule by the method of gene synthesis.
Chromatography, High Pressure Liquid↗
A complete complementary DNA for the oncodevelopmental calcium-binding protein, oncomodulin.
RNA from a rat liver tumor (Morris hepatoma 5123tc) was used to construct cDNAs together comprising the complete coding sequence of rat oncomodulin mRNA. Information obtained from these cDNAs as well as from primer extension analysis gave a deduced length for the complete oncomodulin mRNA of approximately 680 nucleotides (excluding the poly(A) tail) including a 5'-untranslated region of 97 +/- 2 nucleotides, a 324-nucleotide-coding sequence and a 259-nucleotide 3'-noncoding region. Comparison of the oncomodulin cDNA sequence with those coding for other members of the calcium-binding protein family shows little homology with the exception of a recently reported parvalbumin cDNA where the oncomodulin and parvalbumin nucleotide sequences are 59% identical in the protein-coding region. RNA blot analysis of poly(A+) RNA from normal adult rat liver gave no evidence of oncomodulin expression in this tissue. A single RNA species was detected, however, in RNA extracts from the hepatoma and from rat and human placentas. A probe prepared from one of the rat oncomodulin cDNAs hybridized with a single DNA species in restriction digests of hepatoma and normal DNA from rat and sequences in DNA of humans and other mammals. A 38-nucleotide sequence spanning the 5'-untranslated region and the first seven codons of the oncomodulin cDNA, was far less homologous than was the same region of a parvalbumin cDNA, to a chicken calmodulin cDNA sequence coding for the first calcium-binding domain. The oncomodulin gene appears to have diverged more from that of calmodulin than has the parvalbumin gene.
Amino Acid Sequence↗
Genetic mapping, distribution, and properties of an aconitase isozyme in Anopheles albimanus (Diptera:Culicidae).
Electrophoretic analysis of the developmental stages and tissues of Anopheles albimanus showed that qualitatively similar allozymes of aconitase (Acon-2) occur at all stages, and the enzyme is widespread in every larval and adult tissues. Relative heat stabilities of the allozymes were investigated by electrophoresis of heated aqueous extracts and by heating the enzyme in situ in acrylamide gels after electrophoretic separation in Tris-citrate and Tris-maleate buffer systems. The pupal aconitase in the crude extract is more stable to heat than the larval and adult enzyme. The presence of citrate ions in the gel increased the stability of aconitase to heat. Studies of substrate specificities indicated that cis-aconitic acid is the best substrate but citric acid can also serve as a substrate. Zymograms developed with isocitric acid as a substrate showed no aconitase electromorphs and produced only isocitrate dehydrogenase bands. Aconitase has a pH optimum of 8.0 and this enzyme is completely inhibited if treated in situ with ethylenediaminetetra-acetic acid (EDTA), p-chloromercuribenzoate (PCMB), and urea at concentrations higher than 5 mM, 5 X 10(-5) M, and 2 M, respectively. Acon-2(100) and Acon-2(105) do not respond differently to the above treatments. Genetic crosses involving a holandric translocation, pericentric inversions, visible mutants, and allozyme markers were analyzed to map the aconitase (Acon-2) locus on the left arm of chromosome 3. The gene sequence (and map distances) on 3L is centromere-esterase-8 (Est-8)-2-esterase-4 (Est-4)-25-esterase-2 (Est-2)-9-Acon-2-5-phosphoglucomutase (Pgm)-7-esterase-6 (Est-6).
Aconitate Hydratase↗
Extramedullary (skin) presentation of acute monocytic leukemia resembling cutaneous lymphoma: morphological and immunological features.
Acute monocytic leukemia has been noted to exhibit a predilection for extramedullary involvement (gums, skin, and lymph nodes) at presentation. More unusual is the occurrence in an extramedullary site in the absence of bone marrow involvement. A case is reported with initial presentation in skin preceding a subsequent evolution to a leukemic phase by one year. The skin tumor was initially diagnosed and treated as a lymphoma. A second skin tumor, biopsied one year later was immunophenotyped as a T cell lymphoma using a screening panel of antisera (OKT4 positive, OKMI negative). Shortly thereafter a monocytic leukemia (M5) was discovered. Using a larger panel of antisera and enzyme markers on the second skin biopsy confirmed the monocytic rather than lymphocytic nature of the skin tumor. This case illustrates the importance of using an expanded panel of monoclonal antisera in certain hematopoietic tumors.
Bone Marrow Examination↗
Storage and transportation of lymphoid tissue for immunophenotyping.
Immunoperoxidase staining of frozen sections is a cost-effective technic for immunophenotyping cells of lymphoid tissue. Because this procedure is not performed in many institutions, a simple method to transport fresh tissue to centers performing these studies is required. Tissues in saline at refrigerator temperature may be successfully transported. In addition, in order to minimize laboratory expenses, lymphoid tissue can be kept refrigerated in saline until permanent sections are examined and immunodiagnostic procedures become necessary. In this study reproducible immunophenotyping of 12 samples of lymphoid tissue stored up to seven days was achieved.
Antibodies, Monoclonal↗
Myelofibrosis and true histiocytic lymphoma.
A 60-year-old female presented with a history of progressive shortness of breath, fever, and weight loss of 55 pounds. The work-up consisting of computerized axial tomography (CT) scan of thorax and abdomen, mediastinoscopy, and bilateral bone marrow aspiration and biopsy revealed a large-cell or histiocytic lymphoma involving bone marrow with myelofibrosis. Further immunologic and ultrastructural investigation confirmed the true histiocytic origin of the tumor. The patient was treated with 12 courses of intravenous cyclophosphamide, onconvin, doxorubicin, and prednisone and achieved a complete remission with disappearance of clinical symptoms, normal CT scan of thorax and abdomen, and normal bone marrow with disappearance of myelofibrosis from the same site as the previous bone marrow test. At present the patient is in complete remission. We present this case because of the previously unreported association between histiocytic lymphoma and myelofibrosis, and the unusually good response to chemotherapy and the disappearance of fibrosis from the marrow.
Female↗
Malignant lymphoma presenting with prominent splenomegaly. A clinicopathologic study with special reference to intermediate cell lymphoma.
Although non-Hodgkin's lymphoma presenting with prominent splenomegaly is a well-recognized clinical syndrome, previous reports of such cases create confusion today because of the use of outdated pathologic classifications, awkward or inappropriate terms, and imprecise diagnostic criteria. The authors have studied 31 such cases and have classified them according to the modified Rappaport and Lukes-Collins classifications as well as the recently introduced International Working Formulation. Most of our cases (30/31) of malignant lymphoma presenting with prominent splenomegaly were of the small cell type, with morphologic and/or immunologic evidence of B-cell origin. The single largest subtype in our series (19/30) was intermediate lymphocytic lymphoma (IL), a recently described entity in which this mode of presentation has not been previously emphasized. Although such cases have been termed "primary splenic lymphoma," almost all are disseminated diseases that pursue a progressive course and require multiagent chemotherapy and/or radiotherapy.
Adult↗
A novel deletion found during cloning of a synthetic palindromic DNA.
A 212-bp palindromic DNA comprising two copies of the left end of bacteriophage Mu was assembled from chemically synthesized oligonucleotides and inserted into plasmid pUC9. When cloned and propagated in Escherichia coli, the palindrome was found to be unstable and was generally lost. However, in a few cases, a precise, asymmetric deletion of one half of the insert was observed. This pattern of deletion suggests that the symmetry axis region of the palindrome was involved as recognition site in the deletion process.
Bacteriophage mu↗
Genetic and physiochemical studies on beta-hydroxy acid dehydrogenase in Anopheles albimanus.
beta-Hydroxy acid dehydrogenase (beta-Had-2) of Anopheles albimanus was assigned to chromosome 3. The apparent sequence of loci on chromosome 3 is hexokinase-1--22--stripe--28--beta-hydroxy acid dehydrogenase-2--4--aldehyde oxidase--2--esterase-8--4--esterase-4--?--phosphoglucomutase--?--esterase-6. beta-Hydroxy acid dehydrogenase is 25 and 30 map units from phosphoglucomutase and esterase-6, respectively. The one-band electromorph of beta-Had-2 in homozygotes and the three-band type in heterozygotes suggest that the enzyme is a dimer. A variety of electrophoretic techniques and spectrophotometric analysis were used to determine if the allozymes of beta-Had-2 can be differentiated on a basis other than mobility. No differences were detected among the allozymes on the basis of thermostability, urea denaturation, response to thiol reagents, chelating agents, or changes in coenzyme and substrate concentrations. No heterogeneity within allozymes separated by electrophoresis was detected by using thermostability tests.
Animals↗
Genetic mapping and characterization of aldehyde oxidase of Anopheles albimanus (Diptera: Culicidae).
Aldehyde oxidase (Ao) of Anopheles albimanus Wiedemann was mapped on chromosome 3. The sequence is hexokinase-1--19.2 +/- 1.8--stripe--28.3 +/- 2.2--beta-hydroxy acid dehydrogenase--3.6 +/- 0.3--aldehyde oxidase--2.6 +/- 0.4--esterase-8--6.1 +/- 1.9--esterase-4--?--esterase-6 (phosphoglucomutase). Aldehyde oxidase is 26.1 +/- 2.5 from phosphoglucomutase and 27.2 +/- 1.6 from esterase-6. The one-band electromorph of Ao in homozygotes and the three-band type in heterozygotes suggest that the enzyme is a dimer. The isoelectric points of slow and fast allozymes are 5.5 and 4.8, respectively. A variety of electrophoretic techniques was used to determine if the allozymes of Ao can be differentiated on a basis other than mobility. The slow, fast, and hybrid genotypes were analyzed for differences in thermostability, reactivity to thiol reagent, susceptibility to urea denaturation, substrate specificities, and response to chelating agents. The relative effect of p]H on allozymes was tested by varying the pH of the staining buffer over a range of 4-12. No significant differences were detected among allozymes and no additional allelic variations were observed.
Aldehyde Oxidase↗
Synthesis of a human insulin gene. VI. Expression of the synthetic proinsulin gene in yeast.
The construction of plasmid vectors for the controlled expression of a synthetic human proinsulin gene in the yeast Saccharomyces cerevisiae is described. Attempts to express the proinsulin gene using the yeast ADH1 promoter alone did not yield detectable levels of proinsulin. Successful expression was achieved when the proinsulin gene was fused with the promoter and protein leader sequence of the GAL1 gene (coding for yeast galactokinase) in the yeast-Escherichia coli plasmid vector pYT7810. Two different-length leader sequences were employed; the longer leader (about 280 amino acids, fusion plasmid pPS13) gave about five times greater expression than the shorter leader fusion (30 amino acids, plasmid pPS5). Both fusions gave soluble protein products, and the proinsulin could be cleaved by cyanogen bromide treatment from the leader polypeptide. Proinsulin was detected by radioimmunoassay for human C-peptide only in cells induced with galactose, and was not detected in the gene fusions that were out of phase with the GAL1 leader sequence. Methods of improving the level of expression of the proinsulin gene in yeast using this system are discussed.
Amino Acid Sequence↗
Use of a new retrieving adaptor in the cloning of a synthetic human insulin A-chain gene.
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Chemical Phenomena↗