Showing papers in "Basic life sciences in 1984"
TL;DR: Many species of bacteria have genes that control resistances to specific toxic heavy metals, and these resistances often are determined by extrachromosomal DNA molecules (plasmids).
Abstract: Bacteria carry out chemical transformations of heavy metals These transformations (including oxidation, reduction, methylation, and demethylation) are sometimes by-products of normal metabolism and confer no known advantage upon the organism responsible Sometimes, however, the transformations constitute a mechanism of resistance Many species of bacteria have genes that control resistances to specific toxic heavy metals These resistances often are determined by extrachromosomal DNA molecules (plasmids) The same mechanisms of resistance occur in bacteria from soil, water, industrial waste, and clinical sources The mechanism of mercury and organo- mercurial resistance is the enzymatic detoxification of the mercurials into volatile species (methane, ethane, metallic Hg0) which are rapidly lost from the environment Cadmium and arsenate resistances are due to reduced net accumulation of these toxic materials Efficient efflux pumps cause the rapid excretion of Cd2+ and AsO4 3− The mechanisms of arsenite and of antimony resistance, usually found associated with arsenate resistance, are not known Silver resistance is -due to lowered affinity of the cells for Ag+, which can be complexed with extracellular halides, thiols, or organic compounds Sensitivity is due to binding of Ag+ more effectively to cells than to CI−
69 citations
TL;DR: The research reported here describes the statistical properties of HFCs, particularly their utility in detecting low levels of genetic damage which may be undetected by a simple t-test comparing the means of two samples of SCEs.
Abstract: The existence of a subpopulation of lymphocytes in which genetic damage persists was identified in experiments on rabbits injected with low levels of mitomycin C. This led to the suggestion that an important parameter to quantify after exposure to a possibly harmful agent may be the proportion of cells with high sister chromatid exchange (SCE) frequency, i.e., high frequency cells (HFCs). In the research reported here we describe the statistical properties of HFCs, particularly their utility in detecting low levels of genetic damage which may be undetected by a simple t-test comparing the means of two samples of SCEs.
44 citations
TL;DR: There are good prospects for the genetic construction of hybrid haloaromatic catabolic pathways by combining genes encoding broad specificity enzymes, capable of transforming halogenated analogues of their natural substrates, with genes for halocatechol degradation.
Abstract: Halogenated organic compounds constitute one of the largest groups of environmental pollutants and have achieved notoriety as a result of their widespread use despite concerns regarding their toxicity, bioconcentration, and persistence in the biosphere. Government legislation resulting in termination of production of some halogenated aromatics, for example, 2,2-bis (4-chlorophenyl)-1,1,1-trichloroethane (DDT) and the polychlorinated biphenyls (PCBs), has not alleviated problems related to these banned chemicals. According to data presented by Hutzinger and Veerkamp (49), further contamination of the environment may be threatened by PCBs occupying landfills where 22% of total production in the U.S.A. for domestic use since 1929 has been deposited. These authors also suggested that up to 63% of total production is likely still to be present in the environment.
27 citations
TL;DR: While crystallographic work continues in several laboratories, some aspects of the way lysozyme works in solution have been reexamined or clarified, in particular by high resolution NMR work, quantum-chemical calculations, and molecular dynamics calculations.
Abstract: Hen egg-white lysozyme, the most widely studied of the chicken-type lysozymes, is an enzyme containing 129 amino acid residues, and it has been prepared in at least seven crystalline forms. The mechanism of action of lysozyme in cleaving the muco-polysaccharides of certain bacterial cell walls is now well understood, largely as a result of crystallographic investigations; see Imoto et al. (5) for a review. While crystallographic work continues in several laboratories, some aspects of the way lysozyme works in solution have been reexamined or clarified, in particular by high resolution NMR work (3), quantum-chemical calculations (12), and molecular dynamics calculations (9).
27 citations
TL;DR: After 2,4,5-T has been substantially degraded in contaminated soil the titer of AC 1100 rapidly falls to nearly undetectable levels, which indicates that no serious ecological disturbance is likely to result from the application of AC1100.
Abstract: Maintaining the carbon, nitrogen, and sulfur balances in the environment is one of the main tasks of microorganisms in nature; microorganisms degrade most compounds so that their basic elements can be recycled. However, naturally occurring chlorinated hydrocarbons are rather rare (25). Chlorinated synthetic chemicals such as PCBs, dichloro-diphenyl-trichloro-ethane (DDT), and 2,4,5-T, generally are degraded only slowly (20,23,24), mostly through co-oxida-tive metabolism (1,23), The persistence of these compounds is thought to be due to a lack of the ability of microbial cells to derive their energy and cellular constituents from the oxidative metabolism of these compounds (1), Persistence of chemicals in nature will amplify our pollution problems as time progresses, so that even what seems like an insignificant amount of a given chemical, if applied repeatedly, will accumulate until its environmental impact is felt.
26 citations
TL;DR: Cell cycle kinetics by the sister chromatid differential staining method revealed that MMC treatments of FA and normal cells led to a clearly dose-related delay in cell turnover times, the duration of delay being much longer in FA than in normal cells.
Abstract: Many investigators have described strong correlations between the frequency of sister chromatid exchanges (SCEs) in blood lympho cytes and health situations of the blood donor. Recent studies have further shown that cigarette smoking as well as certain genetic factors, can potentiate the cellular response to chemical treatment. The chemical stress method might thus be a sensitive test for quan-titating the cellular damage or defects that have been induced environmentally and genetically.
26 citations
TL;DR: It is reported that fibroblasts from BCNS patients were slightly hypersensitive to X-ray-induced lethality, and GO-irradiated lymphocytes from BC NS patients were found to have a significantly higher level of X-Ray-induced chromosomal aberrations compared with normal cells.
Abstract: Basal cell nevus syndrome (BCNS) is a rare autosomal dominant inherited disorder (1). About 20% of gene carriers develop brain tumors in early childhood. Basal cell nevus syndrome patients are abnormally susceptible to radiation-induced cancer; several patients treated with radio-therapeutic doses have developed large numbers of basal cell tumors in the irradiated field within 6 mo to 3 yr of ex posure (2-5). Featherstone et al. (6) reported that fibroblasts from BCNS patients showed no increased susceptibility to X-ray-induced cell killing; however, GO-irradiated lymphocytes from BCNS patients were found to have a significantly higher level of X-ray-induced chromosomal aberrations (CAs) compared with normal cells. On the other hand, Chan and Little (7) reported that fibroblasts from BCNS patients were slightly hypersensitive to X-ray-induced lethality.
23 citations
TL;DR: The sister chromatid exchange (SCE) test system using human peripheral lymphocytes is proposed as a valuable tool for the cytogenetic monitoring of exposure to potential chemical mutagens in the occupational environment and the results obtained are rather contradictory.
Abstract: The sister chromatid exchange (SCE) test system using human peripheral lymphocytes is proposed as a valuable tool for the cytogenetic monitoring of exposure to potential chemical mutagens in the occupational environment. We examined the SCE frequencies in organic solvent-exposed workers and reviewed the effects of occupational and environmental chemicals on SCE frequencies. The results obtained in these exposed populations are rather contradictory, which may be related to confounding factors, such as personal life style (smoking, drinking, and drugs) of the examinees, tissue culture conditions and the number of subjects examined. We discussed some practical problems for exposure estimation and sample size determination and are led to the following conclusions. 1) The possible combined effects of potential mutagens and cigarette smoking should be taken into consideration when using the SCE test system. 2) Cell cycle kinetic analysis by differential chromatid staining would provide valuable information as a biological indicator for the monitoring of the workers exposed to xenobiotics. 3) By appropriately setting the number of examinees, monitoring would become more efficient in detecting an increased SCE frequency in the exposed populations. Further studies are also required to enhance the sensitivity of the SCE test system for monitoring purposes.
22 citations
TL;DR: An in vivo method of sister chromatid differentiation based on the intraperitoneal injection of bromodeoxyuridine (BrdUrd) previously adsorbed to activated charcoal is described, as well as the protocols for the use of this method in spermatogonial, salivary gland and bone marrow cells.
Abstract: An in vivo method of sister chromatid differentiation based on the intraperitoneal (ip) injection of bromodeoxyuridine (BrdUrd) previously adsorbed to activated charcoal is described, as well as the protocols for the use ot this method in spermatogonial,salivary gland and bone marrow cells, will be presented.
21 citations
TL;DR: The results confirm the opinion that directly induced SSBs can contribute to the induction of CAs in cells with BrdUrd-substituted DNA, but that these SSBs are not efficiently converted to SCEs.
Abstract: The induction of sister chromatid exchanges (SCEs) and chromosomal aberrations (CAs) with bleomycin (BLM), hydrogen peroxide (H/sub 2/O/sub 2/), short- wave ultraviolet (UV)-irradiation, and long-wave UV-irradiation was investigated in V79 cells with BrdUrd-substituted DNA. The application of a Neurospora endonuclease (NE) which specifically cleaves single- stranded DNA after these treatments showed that DNA single-strand breaks (SSBs) are induced by these agents. The SSBs are converted to double- strand breaks (DSBs) by NE and become visible as CAs on metaphase chromosomes. H/sub 2/O/sub 2/ and both types of UV-irradiation also led to an induction of CAs and SCEs, whereas BLM only induced aberrations. Cysteine (Cys) reduced the frequency of the induced SSB-dependent CAs in all treatments, but had no influence on the SCE frequencies after BLM and H/sub 2/O/sub 2/ treatment and had only a slight effect on the UV-induced SCEs. The results confirm the opinion that directly induced SSBs can contribute to the induction of CAs in cells with BrdUrd-substituted DNA, but that these SSBs are not efficiently converted to SCEs. The more recent conceptions regarding the mechanism of SCE are in accordance with these findings and the conclusions derived therefrom. 60 references.
21 citations
TL;DR: The results of these studies have demonstrated that model PCB substrates can be mineralized by indigenous microbial population in contaminated sediments and it remains suspect that transient or trace levels of dissolved oxygen may have permitted conventional aerobic metabolism of the substrate.
Abstract: Interactions between bacterial populations and environmental pollutants which result in the partial or complete biodegradation of the pollutant are of multifaceted importance. Studying these interactions can provide useful information for predicting the persistence of pollutants and needs for discharge and release regulations. Additional information can be obtained to quantify and assess pollutant exposure levels from both ecological and environmental health perspectives. Such studies may also be a source of new bacterial isolates containing genetic information potentially useful for wastewater treatment and pollution abatement. Finally, qualitative and quantitative descriptions of these interactions may provide insights into microbial evolution and natural selection, ranging from the population level to the molecular level. The objective of this report is to review some fundamental concepts and problems related to the microbial ecology of pollutant biodegradation in anaerobic and facultatively anaerobic sediments, and to describe in greater detail current research on the biodegradation of monohalogenated biphenyls (as models for polychlorinated biphenyls) by sediment bacterial populations.
TL;DR: Enhanced SCE induction occurred in older stage embryos, correlating with the increased basal AHH level and enhanced induction capacity of the liver and other organs, and with the findings from in vitro mutation assays that incorporate rat liver S-9 preparations.
Abstract: The embryonic and neonatal periods represent times when the disease process may be initiated as a result of exposure to environ mental mutagens and teratogens. We are using the chick embryo/neo-nate as an experimental system to detect and study the genotoxicity of environmental chemicals in developing tissues and the resultant biological alterations in survivors of perinatal chemical exposure. In vivo bromodeoxyuridine (BrdUrd) labeling of replicating DNA has been employed to measure basal and induced sister chromatid exchanges (SCEs), a candidate cytogenetic endpoint in genetic toxicology testing. Additionally, SCE induction studies with model promu-tagens have permitted the detection and study of components of the developing mixed-function oxidase (MFO) system of the liver and other organs. The relationship between specific MFO enzyme induction and SCE generation by promutagens has been studied in ovo and using in vitro assays.
TL;DR: Findings indicate that studies in axenic animals will be required to elucidate the contribution of the enteric flora to the metabolic activation of some genotoxins.
Abstract: The induction of sister chromatid exchange (SCE) has been proposed as a predictive test for the identification of mutagens/carci-nogens. The in vivo application of this test was investigated by examining the chemical induction of SCE in spermatogonia, intestinal epithelium and bone marrow cells from Chinese hamsters.
TL;DR: Recommendations are given for the preparation of slides under standardized conditions, for the subsequent counting of SCEs/cell in a random sample of 30 cells from each slide, and for the condensation of the information contained in the sample of30 counts into a single statistic, that may be treated as a normally distributed variable.
Abstract: When planning studies by the sister chromatid exchange (SCE) test, it is necessary to calculate the size of the test groups, taking into consideration the variance of the test result and the statistical distribution of SCE frequencies. This paper deals with these problems. Recommendations are given for the preparation of slides under standardized conditions, for the subsequent counting of SCEs/cell in a random sample of 30 cells from each slide, and for the condensation of the information contained in the sample of 30 counts into a single statistic, that may be treated as a normally distributed variable. The adequacy of this transformation is shown for the data from 170 different subjects. Of these, 165 (58 nonsmokers and 107 cigarette smokers) had mean values of SCE/cell ranging from 6.5 to 13.5, while the remaining 5 subjects were on intermittent treatment with cytostatics every fourth wk, and exhibited a mean value of SCE/cell in the range 15-23. The variance associated with the recommended statistic has been decomposed into 4 variance components: variance within slides, variance between slides prepared from the same blood sample, variance within subjects, and variance between subjects. Based on a total of 680 SCE analyses in 218 persons, estimates of these variance components are given and used to calculate the necessary number of samples for the detection of a prescribed difference in SCEs/cell for selected values of Type I and Type II errors.
TL;DR: Search for other sources of intersubject variations in SCEs should continue so that such sources can be controlled in future studies, particularly the human exposure types.
Abstract: While underlying biological mechanisms responsible for sister chromatid exchange (SCE) formation are not fully understood, scientists worldwide are increasingly using SCEs in the evaluation of excess risk from exposure to chemical and biological agents. SCEs are being used as endpoint measures of cell damage in many types of experimental and nonexperimental investigations. The former includes both simple and complex randomized experiments using both animals exposed in vivo and cells exposed in vitro as experimental units. The latter includes the important, yet potentially misleading, human case-control studies in which a group of humans who are or have been exposed to some agent are compared with a selected nonexposed group on SCE frequency. As more is learned about those factors which result in SCE variations, the assay techniques and study protocols can be adjusted to enhance study sensitivity and to minimize potential bias. Although research concerning sample sizes and statistical analysis methods has been conducted, more is needed. Search for other sources of intersubject variations in SCEs should continue so that such sources can be controlled in future studies, particularly the human exposure types. A number of experimental designs are presented and contrasted with their nonexperimental counterparts. Statistical methods are summarized and sample size options are given for the human and animal exposure studies and for the studies in which cells are exposed in vitro.
TL;DR: SCEs and CAs are different cellular phenomena as far as carcinogenesis and the detection of the genotoxic effects of various compounds are concerned, and the relative importance of these two cytogenetical endpoints for mutagenesis and carcinogenesis is considered.
Abstract: There is considerable information currently available about the genotoxic effect, as measured by an alteration in the frequency of sister chromatid exchanges (SCEs), of various environmental chemical compounds (1,13). Evidence is also accumulating on the role of these compounds in carcinogenesis (10) and their ability to induce cytogenetic changes [i.e., chromosomal aberrations (CAs) and SCEs (1,22)]. Considerable information has also been acquired in the* past 10 years about CAs in malignancies, especially hemoblastoses, and there seems to be a close relationship between the location of the break points in specific chromosomal rearrangements and cellular oncogen localization (20). This relationship seems to provide fur ther support to the importance of CA studies in detecting carcinogens, although the role of CAs in tumors and the relationship between the nature of CAs induced by carcinogens and the ones observed in cancer cells remains to be explored. The same lack of understanding, as far as the process of carcinogenesis is concerned, holds true for the relevance of SCEs. Malignant process per se seems not to have an influence on the baseline frequency of SCEs (18), although it is well known that many environmental carcinogens induce SCEs (1) at much lower concentrations of the compounds than is needed for the induction of CAs (16). These marked differences between SCEs and CAs (i.e., their occurrence in malignancies and circumstances of inducibility) underline the fact that SCEs and CAs are different cellular phenomena as far as carcinogenesis and the detection of the genotoxic effects of various compounds are concerned. However, before making any decision as to the relative importance of these two cytogenetical endpoints for mutagenesis and carcinogenesis, one has to realize that most of the studies on CAs have been performed on the tumor tissue, while the information on SCEs in the target tumor tissue is, as yet, very limited (7,17,18).
TL;DR: The present study completes the work published by Camurri et al. (2) and attempts to describe the increase in SCEs at different styrene environmental exposures.
Abstract: Several studies have been published on structural chromosomal aberrations (CAs) in the peripheral lymphocytes of workers in the reinforced plastic industry (1–9). A number of these studies have shown an association between styrene exposure and increased frequen cies of CAs (1–4). Among the studies available on sister chromatid exchange (SCE) induction in the lymphocytes of styrene-exposed workers, only two studies report a slight increase in SCEs (1,2). The present study completes the work published by Camurri et al. (2) and attempts to describe the increase in SCEs at different styrene environmental exposures.
TL;DR: Human mononuclear leukocytes do not activate aniline to genotoxic intermediates capable of inducing SCEs during a 48-hr exposure, but the inclusion of RBCs and granulocytes provides an activation system as demonstrated by a small, but statistically significant increase in the SCE frequency in the whole blood cultures.
Abstract: Erythrocytes [red blood cells (RBCs)] possess aniline hydrox ylase activity. When aniline interacts with ferrohemoglobin in the presence of molecular oxygen, oxidation of nitrogen and ring carbons occurs. Thus, apart from the liver, RBCs may represent an important site of aniline metabolism. Because 2 metabolites of aniline, o-aminophenol and phenylhydroxylamine, can induce sister chromatid exchanges (SCEs), we examined the ability of RBCs and hemoglobin to activate aniline to genotoxic intermediates as evidenced by SCE induction in human lymphocytes. Aniline HC1 (0.05–1.0 mM) induced significant concentration-related increases in the SCE frequency only in the whole blood cultures. Similarly, inhibition of cell cycle kinetics by aniline was observed only in the whole blood cultures, as shown by a concentration-dependent decrease in the percentage of third-(and later) division metaphases. Mitotic indices were not affected significantly at any concentration of aniline or hemoglobin. Hemoglobin (500 or 1,000 ug/ml) alone induced significant concentration-related increases in SCEs in the mononuclear leukocyte cultures. Therefore, human mononuclear leukocytes do not activate aniline to genotoxic intermediates capable of inducing SCEs during a 48-hr exposure. However, the inclusion of RBCs and granulocytes provides an activation system as demonstrated by a small, but statistically significant increase in the SCE frequency in the whole blood cultures. The weak genotoxicity of hemoglobin may be related to production of oxygen radicals during autoxidation to methemoglobin. Thus, a possible mechanism of aniline-induced splenic toxicity in rats may be the combined genotoxic effect of aniline metabolites generated or accumulated in the RBC-engorged spleen and hemoglobin released during phagocytosis of damaged RBCs.
TL;DR: The results support the concept that interphase chromosomes occupy distinct nuclear domains and indicate that the induction of SCEs by UV light is restricted to microirradiated chromatin.
Abstract: Small, medium, and large nuclear areas comprising approximately 5, 30, or 80% of the total area of the interphase nuclei of Chinese hamster cells (M3-1) cultivated in vitro were irradiated with a laser-UV-microbeam of wavelength 257 nm. The DNA of the cells was substituted with 5-bromodeoxyuridine (BrdUrd) for 1 cell cycle in one set of experiments. After microirradiation the cells were grown for a second cycle in medium without BrdUrd (protocol A). In a second set, cells with nonsubstituted DNA were microirradiated and grown for 2 additional cycles, the first in the presence, the second in the absence of BrdUrd (protocol B). In situ chromosome preparation and differential chromatid staining was subsequently performed. The induction of sister chromatid exchanges (SCEs) was found to be dependent on both the ultraviolet (UV) dose and the spatial distribution of the UV energy within the cell nucleus. Following both protocols the average number of chromosomes with SCEs was significantly higher after microirradiation of a large nuclear area as compared to microirradiation of a small nuclear area. In the latter case, multiple SCEs were noted on individual chromosome arms at the first postirradiation mitosis (protocol A). In other cells, especially at higher doses, protocol A resulted in shattering of a few closely neighbored chromosomes which were surrounded by intact ones with normal SCE levels. Microirradiation of medium-sized nuclear areas produced high levels of SCEs over a number of chromosomes which still appeared spatially related in a part of the metaphase spread. Finally, high SCE levels could be observed over most or all chromosomes when a large nuclear area (up to 100%) was exposed to the microbeam. Following protocol B the increase of SCEs was much less pronounced. Microirradiation of a small part of the cytoplasm in addition to the nuclei did not induce SCEs. Our results support the concept (i) that interphase chromosomes occupy distinct nuclear domains and indicate (ii) that the induction of SCEs by UV light is restricted to microirradiated chromatin.
TL;DR: S-9 mixes from sources other than the liver have only seldom been used in mutagenicity tests, and the ratio between activation and inactivation may be an important parameter in determining the target tissue of a precarcinogen.
Abstract: Microsomal metabolism has proved to be essential for the acti vation of many chemical carcinogens. For this reason in vitro mutagenicity tests include a metabolic activation system. As a rule, the metabolizing mixtures are prepared from the postmitochondrial fraction of rodent liver. While it is generally accepted that the liver is the primary organ of xenobiotic metabolism for a number of chemicals, it is also known that other tissues can contribute both to the activating and inactivating reactions. The ratio between activation and inactivation may be an important parameter in determining the target tissue of a precarcinogen. However, S-9 mixes from sources other than the liver have only seldom been used in mutagenicity tests.
TL;DR: This hypothesis revision includes a model that centers on the idea that the sum of the conformational alterations of the DNA polymerase-DNA template complex at replication is the controlling factor in SCE formation.
Abstract: This communication describes the use of 6 different halogenated pyrimidine analogues, bromodeoxyuridine (BrdUrd), chlorodeoxyuridine (CldUrd), iododeoxyuridine (IdUrd), bromodeoxycytidine (BrdCyd), chlorodeoxycytidine (CldCyd), and iododeoxycytidine (IdCyd), to achieve sister chromatid differentiation (SCD) and evaluate sister chromatid exchange (SCE) formation in mitogen-stimulated human lymphocytes. Also included are a description of an in vivo experiment with BrdUrd, CldUrd, and IdUrd; a discussion of pyrimidine metabolism effects on SCEs; and the presentation of an update on the "conformation hypothesis" for SCE formation. This hypothesis revision includes a model that centers on the idea that the sum of the conformational alterations of the DNA polymerase-DNA template complex at replication is the controlling factor in SCE formation.
TL;DR: SCE appears to be a sensitive assay for monitoring the in vivo exposure of individuals to genotoxic agents and there was no relationship between SCE and cell cycle kinetics.
Abstract: The ability of various cytostatic drugs to induce sister chromatid exchanges (SCE) and to alter the progression of cells through mitosis was analyzed in lymphocytes cultured from cancer patients following various in vivo chemotherapy treatments. Control individuals exhibited 4.87 ± 0.08 SCEs per metaphase. Patients being treated with cyclophosphamide (CP), mitomycin C (MMC), and/or cisplatinum (CPT) in combination with other drugs exhibited 3-to 5-fold greater levels of SCEs. Other cytostatic drugs: the plant alkaloids; vincristine (VCR); and homoharringtonine (HHT); the antibiotic, adriamycin (ADM); the folic acid antagonist, methotrexate (MTX); and the nucleotide analogue, dihydroazacytidine (HAC) did not appear to induce SCE levels significantly above controls. Most of the cytostatic drugs used in cancer patients appeared to delay the progression of cells through mitosis. All the drug protocols which included a known DNA-damaging agent induced SCE. There was no relationship between SCE and cell cycle kinetics. Thus, SCE appears to be a sensitive assay for monitoring the in vivo exposure of individuals to genotoxic agents.
TL;DR: The principle of contrast variation can be used in low resolution neutron diffraction to achieve the nucleosome core particle and the distinction between protein and DNA is made.
Abstract: The nucleosome core particle may be regarded as a basic structural unit of chromatin and thus of the chromosome. It is obtained by micrococcal nuclease digestion of chromatin and consists of about equal weights of DNA (146 base pairs) and protein (an octamer of two pairs each of the histones H2A, H2B, H3, and H4). Nucleosome structure has been reviewed by McGhee and Felsenfeld (6). Studies by small-angle neutron scattering using D2O/H2O contrast variation have given the overall dimensions of the nucleosome and have shown that the protein forms an inner core with the DNA located at the outer regions of the molecule (7,12). The x-ray crystal structure of the nucleosome core particle has been solved in projection to a resolution of about 25 A (3). Although this has given a more detailed description of the overall shape of the molecule than has solution scattering, the distinction between protein and DNA is not made. In this paper we show how the principle of contrast variation can be used in low resolution neutron diffraction to achieve this end.
TL;DR: Despite the many recent advances in various aspects of genetic engineering, application of the technology to waste/wastewater treatment is still in its infancy and the ways in which genetic engineering can be most effectively applied to Waste/ wastewater are as yet poorly defined.
Abstract: Despite the many recent advances in various aspects of genetic engineering, application of the technology to waste/wastewater treatment is still in its infancy. The genetics of microorganisms important in biological treatment is almost unknown except for that of the most common organisms, and the state of the art is to a large extent still in the laboratory (1–12). In addition, the ways in which genetic engineering can be most effectively applied to waste/ wastewater are as yet poorly defined.