text:
Columnists/Editorials
Bulloch History with Roger Allen - Coleman's take over the Herald
The Turner Brothers (A.C. and D.B.) controlled, in addition to the Bulloch Herald, rights to three more papers: the Bulloch Times, the Statesboro News, and the Statesboro Star. In 1917, these three papers were then combined into a single paper, the Bulloch Times, and then sold shortly thereafter to the Millers.
The Miller brothers (James and Frank) combined the Bulloch Times, Statesboro News, and the Statesboro Eagle into one single paper, the Bulloch Times, in 1920. Then, J. Shields Kenan, owner of the Kenan Publishing Company in Statesboro, bought the rights to the Bulloch Times and began printing the paper at his own shop.
Meanwhile, in 1924 at the Georgia Normal School, students and faculty had begun their first publication, which they called Station GNS. This paper was succeeded by the Reflector in 1926, which in turn was replaced in 1927 by the George-Anne. This college newspaper is now the longest continuously published newspaper in Bulloch County.
On March 26, 1937, the Coleman family started publication of the long-suspended Bulloch Herald. Leodel Coleman was the Editor, G.C. Jr. was the Associate Editor, and Jim was the Advertising Director. The first three issues of the paper were printed at the Swainsboro Forest Blade and the fourth edition was printed by the Vidalia Advance.
In 1939, the Colemans bought the Banner Publishing Company, and moved the newspaper to the Banner Building in Statesboro. In 1942, the Bulloch Herald suspended publication for the duration of World War Two, as all three Colemans had each joined different branches of the armed forces.
Leodel became a Marine Corps Combat Correspondent; Jim joined the Air Force; and G.C. Jr. became an Army Paratrooper. The Bulloch Herald was restarted in 1946 by the Colemans only after all three brothers had returned safely from the war.
In 1957, the Bulloch Herald was merged with the Bulloch Times, to form what was called simply the Bulloch Herald and Times. In 1962 Kenan ceased being the publisher, although the paper continued to be published as the Bulloch Herald and Times until 1970.
From 1970 until 1983, the Southern Beacon was published in Statesboro, at which time its name was shortened to simply the Beacon for the last three years of its existence. Not long after the Beacon closed, another paper emerged. Known as the Statesboro Georgian, this paper served the Statesboro public from 1988 until 1992.
The Bulloch Herald and Times name was changed to the Statesboro Herald in 1970, and is the name the newspaper still bears today. In addition to the regular Statesboro Herald, from February through June of 1994 the Statesboro Herald Extra Express was published as well.
Roger Allen is a local lover of history. Allen provides a brief look at Bulloch County's historical past. E-mail Roger at rwasrer53 @gmail.com


A lot has happened since the steam engine changed the course of our civilization history with the mechanization of production in the First Industrial Revolution. Scientific advances at the end of the 19th century allowed the Second Industrial Revolution with the discovery of electricity that would be the basis for mass production, followed by a Third Industrial Revolution in the 20th century thanks to the power of information technology and electronics in the automation of production processes.
Today, a Fourth Industrial Revolution is brewing, a product of the merge of a series of exponential technologies such as Big Data, Artificial Intelligence, the Internet of Things (IoT), additive manufacturing, augmented reality, among others, which are blurring the barriers between the physical and the digital.
A lot is said about this new stage of the industry. Already, large corporations are moving to adapt to the changes that this entail and are beginning to extract benefits around Industry 4.0. Hence, to understand why this revolution is so unique, we need to realize the role we have as individuals in this new paradigm shift.
The great difference of the Fourth Industrial Revolution, is that is not a cause of change but a consequence. In the case of the Second Industrial Revolution, it resulted as a consequence of the introduction of mass production. It was the revolution that brought the change in the mode of consumption, while the Fourth Revolution is being forged, to a large extent, as a consequence of the new consumption habits of the people. The customization of mass production is the catalyst for the change that, among other things, originates Industry 4.0.
The change in consumption means that it is no longer enough for the product to be as cheap as possible, but also that the product must adapt to everything we need as consumers and what we demand according to our tastes. All in one click and with free shipping. And this is precisely the great change that has forced companies to find more agile and fast solutions that respond to their customers, now hyperconnected, accustomed to booking a flight, asking for a taxi or making a payment, all remotely.
From the point of view of the industry, the change not only consists of the eternal quest to save production costs, but to respond personally and quickly to their consumers. The solution has been found in the digitization of everything; from design to manufacturing.
Digitization brings a key fact; with all being connected, an infinite amount of data is generated, extremely useful to know more and better both, the production chain and the customer. Therefore, having an impact not only improving the operational efficiency but also the generation of new revenues towards the final consumer.
Previously, if a problem arose during the manufacturing process, the whole production chain had to stop to evaluate where the problem was, to fix it, and start it up again. This involved substantial economic losses for every minute the production chain was stopped. The same thing happened when some maintenance of the machines had to be done, always with fixed dates and without taking into account whether it was really necessary or not. Now the new connected industry would prevent the processes from stopping. If everything is communicated, and information is available in real time, we are able to modify actions and predict failures before they pose a real problem, causing to stop the production process.
Thanks to Big Data technologies we are able to carry out predictive maintenance of machines and processes, thus guaranteeing greater efficiency within the industry.
Of course, these changes do not come with insurance at all risk, and therefore we must pay the consequences of automation; employment. According to the study "World Bank Development Report (2016), machines could replace 57% of average jobs in OECD countries, 69% in India and up to 77% in China. Therefore, it affects more, those countries where traditional industry has a leading role. Another study; The Future of Employment (2013) speaks about other sectors; a telemarketer has a 99% chance of being replaced by automation; a supermarket cashier 98%, a legal assistant 94%, a taxi driver 89% even a chef of a fast food chain 81%.
These forecasts only show static data of one side of the coin. The reality is that we will seek to adapt the change and dominate it; new professional profiles will emerge. Profiles such as "Community Manager" for example, were unthinkable a decade ago, or the Data Science discipline. But in the not so distant future we will speak about specialized lawyers in drones and cybersecurity or organ designers. What is clear is that in the future, human skills will prevail over the knowledge of something in particular. A person will be valued more when it comes to being hired for their leadership or management skills, or their creativity over their knowledge about anything that apart from changing at great speed is accessible to everyone through a mobile device.


text:
Reaction mass of Trisodium tris(D-gluconato(2-)-κO1,κO2)ferrate(3-) and Sodium chloride
Genetic toxicity in vitro
Effects (aneuploidy) were induced by Fe-EDTA at high, non-physiological and/or cytotoxic concentrations after prolonged incubation (20h) in an in vitro screening system. Overall findings indicate that EDTA-FeNa lacks genotoxic potential under conditions that do not deplete essential trace elements required for normal cell function.
In a weight of evidence approach it can be concluded that the effects induced in in vitro assays by some metal EDTA's are linked to zinc depletion after prolonged incubation and/or cytotoxicity. Both situations might be relevant for an in vitro situation. However, the effect is considered irrelevant to humans, as a considerable and sustained zinc depletion is required to induce cytotoxic/genotoxic effects, which is impossible to achieve at relevant human exposure levels. Furthermore, it is demonstrated in studies using Zn-EDTA as test substance or in studies using zinc depletion/repletion protocols, that DNA-damaging effects are not induced if zinc homeostasis is not disturbed.
No in vitro genotoxic effects were observed for Na-glucoheptonate.
Referenceopen allclose all
in vitro cytogenicity / micronucleus study
Type of genotoxicity: chromosome aberration
read-across from supporting substance (structural analogue or surrogate)
May-August 2010
other: Well conducted study according to GLP
Justification for type of information:
REPORTING FORMAT FOR THE ANALOGUE APPROACH
read-across source
other: draft OECD guideline 487
Type of assay:
in vitro mammalian cell micronucleus test
Species / strain / cell type:
lymphocytes: human
Metabolic activation:
Metabolic activation system:
Aroclor 1254-induced rat liver homogenate
Test concentrations with justification for top dose:
First test (4h, with and without S9-mix): 7.8, 15.6, 31.3, 62.5, 125, 250, 500, 1000, 2000, 4211 µg/mL
Second test (20 h, without S9-mix): 10, 50, 125, 250, 500, 1000, 1500, 2000, 2500, 3000, 4211 µg/ml
Vehicle / solvent:
culture medium
Negative solvent / vehicle controls:
Positive controls:
Positive control substance:
other: Mitomycin C (clastogen) and Vinblastine sulphate (aneugen)
without S9-mix
cyclophosphamide
with S9-mix Migrated to IUCLID6: (clastogen)
Details on test system and experimental conditions:
Blood samples for the first and second test were obtained by venapuncture from a young female (27 years old) and a young male (35 years old), respectively. Both blood donors were healthy non-smoking persons with no known recent exposures to genotoxic chemicals or radiation. The blood was collected in sterile, heparinized vacutainer tubes and gently mixed before use to prevent clotting. The cultures were set up within 1 hour after withdrawal of the blood.
Evaluation criteria:
Species / strain:
Genotoxicity:
Cytotoxicity / choice of top concentrations:
cytotoxicity
Vehicle controls validity:
Positive controls validity:
Remarks on result:
Migrated from field 'Test system'.
Test 1: Observed cytotoxicity
In the presence of metabolic activation, all dose levels analysed (4211, 2000, 1000, 500, 250 and 125 μg/ml) showed 38%, 24%, 17%, 28%, 12% and 11% toxicity, respectively. In the absence of metabolic activation, all dose levels analysed (4211, 2000, 1000, 500, 250 and 125 μg/ml) were slightly toxic to the cells and showed 13%, 13%, 18%, 5%, 9% and 13% toxicity, respectively. The positive control substances Cyclophosphamide (20 μg/ml), Mitomycin C (0.4 μg/ml) and Vinblastine sulphate (0.025 μg/ml) showed 64%, 55% and 9% toxicity, respectively.
Test 1: Micronuclei induced by the test substance
Three dose levels (1000, 2000 and 4211 µg/mL) and the controls were analysed for micronuclei. In the presence and absence of a metabolic activation system (S9-mix), pulse treatment (4 hours) with the test substance did not result in a statistically significant increase in the number of binucleated cells containing micronuclei, at any of the concentrations analysed, when compared to the numbers found in the concurrent control cultures.
As a result of continuous treatment with the test substance the two highest dose levels analysed (4211 and 3000 μg/ml) showed severe toxicity of 76% and 69%, respectively. The four next lower dose levels analysed (2500, 2000, 1500 and 1000 μg/ml) were clearly to slightly toxic to the cells and showed 57%, 41%, 31%, 23% and 6% toxicity, respectively. At the lowest dose levels analysed (250, 125, 50 and 10 μg/ml) no toxicity was observed. The positive control substances Mitomycin C (0.05 μg/ml) and Vinblastine sulphate (0.025 μg/ml) showed 25% and 19% toxicity, respectively.
Four dose levels of the test substance (2500, 1500, 500 and 125 μg/ml), ranging from 55 ± 5% toxicity to no toxicity, together with the negative and positive controls, were analysed for micronuclei formation in binucleated lymphocytes. Continuous treatment with the test substance for 20 hours resulted in a statistically significant increase in the number of binucleated cells containing micronuclei at one dose level (2500 μg/ml; ***p<0.001) with high (55 ± 5%) but acceptable toxicity, at one moderate dose level (1500 μg/ml; ***p<0.001) with average toxicity and at one low dose level (500 μg/ml; *p<0.05) with slight toxicity, when compared to the numbers found in the concurrent control cultures. At the lowest dose level (125 μg/ml), the test substance did not induce a statistically significant increase in the number of binucleated cells containing micronuclei, when compared to the number found in the concurrent negative control (culture medium).
Test 2: Size-classified micronucleus counting
To discriminate aneugens from clastogens from in vitro micronucleus test positive compounds, size-classified micronucleus counting was performed on the slides of all dose levels of the test substance with statistically significant increases in the number of binucleated cells containing micronuclei (2500, 1500 and 500 μg/ml), together with the slides of the positive controls Mitomycin C and Vinblastine sulphate. The proportion of large micronuclei, found at the three test substance dose levels (2500, 1500 and 500 μg/ml) were 38%, 42% and 18%, respectively, which was greater than the border (10 ± 2%) between aneugens and clastogens 10 ± 2%. The test substance EDTA-FeNa clearly increased the proportion of large micronuclei at all dose levels analysed. The relatively small proportion (9%) of large micronuclei induced by the clastogen Mitomycin C and the relatively large proportion (34%) of large micronuclei induced by the aneugen Vinblastine sulphate, demonstrated the expected response of a clastogen and aneugen, respectively and were comparable with data presented in literature.
Interpretation of results (migrated information):
positive without metabolic activation
The results of the first in vitro micronucleus test with EDTA-FeNa in human lymphocytes was negative following 4 h exposure with and without metabolic activation. The 2nd test (20- h treatment without metabolic activation) was positive. Based on the results of the size-classified micronucleus counting in the
second micronucleus test, EDTA-FeNa clearly increased the proportion of large micronuclei at three dose levels, at acceptable toxicity levels. This increased
proportion of large micronuclei is considered to be an indication for aneugenic effects, under the conditions used in this study.
The test substance EDTA-FeNa was examined for its potential to induce micronuclei in cultured binucleated human lymphocytes, in both the absence and presence of a metabolic activation system (S9-mix) with duplicate cultures. The micronucleus study consisted of two separate tests for which blood was obtained from two different donors. In the second test, size-classified micronucleus counting was additionally performed on the slides of three dose levels of the test substance and the positive controls Mitomycin C and Vinblastin sulphate, to discriminate aneugens from clastogens.
In the first test, in the presence and absence of metabolic activation (S9-mix) the treatment time was 4 hours (pulse treatment) and the recovery time 20 hours. In the second test, in which metabolic activation was absent and concentration spacing was modified, the treatment time was 20 hours (continuous treatment) and the recovery time 28 hours. Dose levels of the test substance ranging from 7.8 to 4211 μg/ml were tested in the culture medium. In all instances, the maximum final concentration in the culture medium was 10 mmol/l. Culture medium was used as solvent for the test substance. Cytotoxicity was calculated from the Cytokinesis- Block Proliferation Index (CBPI). Based on cytotoxicity, at least three dose levels
were selected for micronuclei analysis. Cyclophosphamide, a clastogenic compound which requires metabolic activation, was used as positive control in the presence of S9-mix. A known clastogenic compound (Mitomycin C) and a known aneugenic compound (Vinblastine sulphate) were used as positive controls in the absence of S9-mix.
In the first test, in both pulse treatment groups, analysis of micronuclei formation was carried out in the cultures of three dose levels of the test substance (4211, 2000 and 1000 μg/ml), the cultures of the solvent control (culture medium) and the cultures of the positive controls. The test substance did not induce a statistically significant increase in the number of binucleated cells containing micronuclei, at any of the dose levels analysed, when compared to the numbers found in the concurrent negative control (culture medium).
In the second test, after continuous treatment with the test substance, analysis of micronuclei formation was carried out in the cultures of four dose levels (2500, 1500, 500 and 125 μg/ml) of the test substance, the cultures of the solvent control (culture medium) and the cultures of the positive controls. At the three highest dose levels analysed, the test substance induced a statistically significant increase (p<0.001 at 2500 μg/ml and 1500 μg/ml; p<0.05 at 500 μg/ml) in the number of binucleated cells containing micronuclei, when compared to the numbers found in the concurrent negative control (culture medium). At the lowest dose level analysed (125 μg/ml), the test substance did not induce a statistically significant
increase in the number of binucleated cells containing micronuclei, when compared to the number found in the concurrent negative control (culture
medium).
To discriminate aneugens from clastogens from in vitro micronucleus test positive compounds, size-classified micronucleus counting was performed on the slides of all dose levels with a statistically significant increase in the number of binucleated cells containing micronuclei (2500, 1500 and 500 μg/ml), together with those of the positive controls Mitomycin C and Vinblastine sulphate. The proportions of large micronuclei, found at the three test substance dose levels analyzed (2500, 1500 and 500 μg/ml) were 38%, 42% and 18%, respectively which were greater than the border (10 ± 2%) between aneugens and clastogens. The test substance EDTA-FeNa clearly increased the proportion of large micronuclei at all dose levels analysed. The relatively small proportion (9%) of large micronuclei induced by the clastogen Mitomycin C and the relatively large proportion (34%) of large micronuclei induced by the aneugenVinblastine sulphate demonstrated the expected response of a clastogen and aneugen, respectively and were comparable with data presented in literature.
In both the first and second test, with respect to the formation of micronuclei, the negative controls were comparable with the data presented in the literature and the historical data. Treatment with the positive controls Cyclophosphamide, Vinblastine sulphate and Mitomycin C resulted in statistically significant increases in the numbers of binucleated cells containing micronuclei, when compared to the numbers observed in the cultures treated with the solvent control. This demonstrates the validity of both the first and second in vitro micronucleus test.
In the second test, with respect to the size-classified micronucleus counting, treatment with the positive controls Mitomycin C and Vinblastine sulphate resulted in an expected small and large proportion of large micronuclei, respectively. This demonstrates the validity of the size-classified micronucleus counting carried out in the second in vitro micronucleus test.
Based on the results obtained in two in vitro micronucleus tests, the test substance EDTA-FeNa induced a statistically significant increase in the number of binucleated cells containing micronuclei in the second test (continuous treatment), when compared to the negative control (culture medium), under the conditions used in this study. Based on the results of the size-classified micronucleus counting in the second test (continuous treatment), EDTA-FeNa clearly increased the proportion of large micronuclei at three dose levels, at acceptable toxicity levels. This increased proportion of large micronuclei is considered to be an indication for aneugenic effects, under the conditions used in this study.
in vitro gene mutation study in bacteria
Type of genotoxicity: gene mutation
other: The study was performed according to methods similar to OECD471, non-GLP. However the reporting of results for EDTA-FeNa is limited.
OECD Guideline 471 (Bacterial Reverse Mutation Assay)
other: Ames te al. 1975 and Yahagi et al. 1977
bacterial reverse mutation assay
Target gene:
Histidine operon
S. typhimurium TA 1535, TA 1537, TA 98 and TA 100
S. typhimurium TA 102
other: TA 97a
S9 mix
up to 10,000 µg/Fe plate = 75,397.76 µg EDTA-FeNa/plate
- Vehicle(s)/solvent(s) used: distilled water
Untreated negative controls:
True negative controls:
METHOD OF APPLICATION: in agar (plate incorporation) and preincubation
- Preincubation period: 20 minutes
- Exposure duration: 48 hours
SELECTION AGENT (mutation assays): histidine
NUMBER OF REPLICATIONS: triplicate
NUMBER OF CELLS EVALUATED: all plates were examined for revertant colonies
DETERMINATION OF CYTOTOXICITY
- Method: growth rate
The criteria used to evaluate a test stipulated that a test article must induce at least a doubling in the mean number of revertants per plate of at least
one tester strain (TA97a, TA98, TA100, TA102, and TA1535) for it to be considered positive. This increase in the mean revel (ants per plate must be accompanied by a dose response to increasing concencmtions of the test chemical. If the stody shows a dose-response, but with a less than 3-fold increase on TA1537 or TA1538, the response must be confirmed in it repeat experiment.
other: all strains tested
Untreated negative controls validity:
Additional information on results:
EDTA-FeNa tested up to 10,000 µg/plate Fe in the plate incorporation and pre-incubation Ames test dit not result in an increased number of revertant colonies in strains S. typhimurium strains TA 98, 97a., 100, 102, 1537, 1538.
EDTA-FeNa tested up to 10,000 µg/plate Fe in the plate incorporation and pre-incubation Ames test dit not result in increased number of revertant colonies in strains S. typhimurium strains TA 98, 97a., 100, 102, 1537, 1538.
in vitro gene mutation study in mammalian cells
other: The study was performed according to methods similar to OECD471, non-GLP
OECD Guideline 476 (In Vitro Mammalian Cell Gene Mutation Test)
other: Clive and Spector 1975
mammalian cell gene mutation assay
thymidine kinase (TK) deficiency
mouse lymphoma L5178Y cells
Details on mammalian cell type (if applicable):
- Type and identity of media: The cells wcre grown in Fischer's medium for leukemic cells of mice (Irvine Scientific, Irvine, CA) supplemented with 10% horse serum (Hyclone Laboratories, Logan, UT) and 0.02% pluronic F-68 (BASF Wyandotte Corp., Wyandotte, MI).
- Properly maintained: yes
- Periodically checked for Mycoplasma contamination: yes
- Periodically checked for karyotype stability: no data
- Periodically "cleansed" against high spontaneous background: no data
New cultures were initiated at approximately 3-month intervals rrom cells stored in liquid N2.
Additional strain / cell type characteristics:
EDTA-FeNa
- S9 mix
0, 1.3, 2.6, 162.5, 325.0 µg Fe/ml = 0, 9.80, 19.60, 1225.21, 2450.43 EDTA-FeNa
+ S9 mix
0, 0.026, 0.052, 1.625, 3.250 µg Fe/ml = 0, 0.20, 0.39, 12.25, 24.50
(mol weight Fe 55.847, mol weight EDTA-FeNa 3H2O 421.096)
EDTA-Na2
0, 250, 500, 1000, 1500, 2000 µg/ml
0, 250, 500, 1000, 1500, 2000, 4000 µg/ml
other: EDTA-FeNa: -S9 mix 4.7*10-6M EMS, +S9mix 9*10-5M MCA, EDTA-Na2: -S9 mix 0.25 µg/ml EMS, +S9mix 5.0 µg/ml 3-MCA
EDTA-Na2 was used as non-Fe contaning control compound
METHOD OF APPLICATION: in medium
- Exposure duration: 4 hours
- Expression time (cells in growth medium): 48 hours
- Selection time (if incubation with a selection agent): 10-12 days
- Fixation time (start of exposure up to fixation or harvest of cells): 292-340 hours
SELECTION AGENT (mutation assays): TFT
NUMBER OF REPLICATIONS: duplicate
NUMBER OF CELLS EVALUATED: colonies > 0.1 mm were counted.
Doubling of the mutant frequency over the concurrent solvent-treated control value as an indication of a positive effect, together with evidence
of a dose-related increase.
-S9 mix >2.6 µg Fe/ml, + S9 mix >0.052 µg Fe/ml
+S9 mix > 2000 µg/ml
TEST-SPECIFIC CONFOUNDING FACTORS
- Effects of pH: no data
- Effects of osmolality: no data
- Evaporation from medium: no data
- Water solubility: no data
- Precipitation: no data
- Other confounding effects: no data
RANGE-FINDING/SCREENING STUDIES: study was performed, results not reported.
COMPARISON WITH HISTORICAL CONTROL DATA: no data
ADDITIONAL INFORMATION ON CYTOTOXICITY: no data
The authors of this study concluded that EDTA-FeNa is positive in the mouse lymphoma mutagenicity study. However doubling of the number of mutants is only observed at test concentrations that cause significant cytotoxicity. Not taking into account the cytotoxic concentrations does not give a dose related increased in mutant frequency. OECD476: "Care should be taken to avoid conditions which would lead to results not reflecting intrinsic mutagenicity. Positive results which do not reflect intrinsic mutagenicity may arise from changes in pH, osmolality or high levels of cytotoxicity." Therefore we concluded that the results from this study are ambiguous.
The mutagenic activity of EDTA-FeNa and EDTA-Na2 was tested in a mammalian gene mutation assay with L5178Y mouse lymphoma cells. The authors of this study concluded that EDTA-FeNa is positive in the mouse lymphoma mutagenicity study. However doubling of the number of mutants is only observed at test concentration that cause significant cytotoxicity. Not taking into account the cytotoxic concentrations does not give a dose related increased in mutant frequency. EDTA-Na2 is much less cytotoxic and is negative in this assay.
no adverse effect observed (negative)
Genetic toxicity in vivo
Two Chinese in vivo genotoxicity studies, although with major flaws such as lack of details, no GLP, and no official translation, did not show genotoxicity of EDTA-FeNa up to oral doses of 400 mg/kg bw. No in vivo genotoxic effects were seen with Na-glucoheptonate.
in vivo mammalian somatic cell study: cytogenicity / erythrocyte micronucleus
The experimental phases of the study were performed between 28th February 2012 and 11th December 2012.
other: Study conducted in compliance with agreed protocols, with no or minor deviations from standard test guidelines and/or minor methodological deficiencies, which do not affect the quality of relevant results.
OECD Guideline 474 (Mammalian Erythrocyte Micronucleus Test)
EU Method B.12 (Mutagenicity - In Vivo Mammalian Erythrocyte Micronucleus Test)
EPA OPPTS 870.5395 (In Vivo Mammalian Cytogenetics Tests: Erythrocyte Micronucleus Assay)
micronucleus assay
Sufficient albino Hsd: ICR (CD-1®) strain mice were obtained from Harlan Laboratories UK Ltd., Oxon, UK. At the start of the main test the mice weighed 21 to 30g and were approximately six to ten weeks old. After a minimum acclimatisation period of five days the animals were selected at random and given a number unique within the study by tail marking and a number written on a colour coded cage card.
The animals were housed in groups of up to seven in solid-floor polypropylene cages with wood-flake bedding. Free access to mains drinking water and food (Harlan Teklad 2014C Global Certified Rodent Diet supplied by Harlan Laboratories UK Ltd., Oxon, UK) was allowed throughout the study.
The temperature and relative humidity were set to achieve limits of 19 to 25°C and 30 to 70%, respectively. Any occasional deviations from these targets were considered not to have affected the purpose or integrity of the study. The rate of air exchange was approximately fifteen changes per hour and the lighting was controlled by a time switch to give twelve hours light and twelve hours darkness.
intraperitoneal
The vehicle was supplied as a 10x concentrated solution by Gibco, as follows:
Supplier's identification : Dulbecco's Phosphate Buffered Saline Solution
Supplier's lot number: 938281
In-house serial number : V-5241
Date received : 02 November 2011
Expiry date : 01 May 2013
Storage conditions : Room temperature
A range-finding toxicity test was performed to determine a suitable dose level and route of administration for the micronucleus test. The dose level selected should ideally be the maximum tolerated dose level or that which produces some evidence of toxicity up to a maximum recommended dose of 2000 mg/kg. The range-finding toxicity test was also used to determine if the main test was to be performed using both sexes or males only. With no evidence of toxicity via the oral route, and following discussions with the Sponsor, it was considered necessary to investigate the intraperitoneal route of administration to maximise exposure of the test item.
24 or 48 hours
Groups, each of seven male mice, were dosed once only via the intraperitoneal route with the test item at 2000, 1000 or 500 mg/kg. One group of mice from each dose level was killed by cervical dislocation 24 hours following treatment and a second group dosed with test item at 2000 mg/kg was killed after 48 hours.
Post exposure period:
Immediately following termination (i.e. 24 or 48 hours following dosing), the animals were dissected and the slide preparation had begun.
2000, 1000 or 500 mg/kg
nominal conc.
7 males per dose group (2000, 1000 or 500 mg/kg)
Two additional groups of male mice were included in the study; one group (seven mice) was dosed via the intraperitoneal route with the vehicle alone (PBS).
A second group (five mice) was dosed orally with cyclophosphamide. Cyclophosphamide is a positive control item known to produce micronuclei under the conditions of the test.
yes, concurrent vehicle
Positive control(s):
The positive control item was supplied by Acros Organics, as follows:
Supplier's identification: Cyclophosphamide
Supplier's lot number : A0302605
In-house serial number : R-5359
Date received : 27 April 2012
Expiry date : 27 April 2014
Storage conditions: Approximately 4°C in the dark
For the purpose of this study the positive control item was freshly prepared as required as a solution at the appropriate concentration in distilled water.
Tissues and cell types examined:
Immediately following termination (i.e. 24 or 48 hours following dosing), both femurs were dissected from each surviving animal, aspirated with foetal bovine serum and bone marrow smears prepared following centrifugation and re-suspension.
Details of tissue and slide preparation:
Immediately following termination (i.e. 24 or 48 hours following dosing), both femurs were dissected from each surviving animal, aspirated with foetal bovine serum and bone marrow smears prepared following centrifugation and re-suspension. The smears were air-dried, fixed in absolute methanol, stained in May-Grunwald/Giemsa, allowed to air-dry and a cover slip applied using mounting medium.
Stained bone marrow smears were coded and examined blind using light microscopy at x1000 magnification. Where possible, the incidence of micronucleated cells per 2000 polychromatic erythrocytes (PCE-blue stained immature cells) per animal was scored. Micronuclei are normally circular in shape, although occasionally they may be oval or half-moon shaped, and have a sharp contour with even staining. In addition, the number of normochromatic erythrocytes (NCE-pink stained mature cells) associated with 1000 erythrocytes was counted; these cells were also scored for incidence of micronuclei. The ratio of polychromatic to normochromatic erythrocytes was calculated together with appropriate group mean values and standard deviations.
A comparison was made between the number of micronucleated polychromatic erythrocytes occurring in each of the test item groups and the number occurring in the vehicle control group.
A positive mutagenic response would be demonstrated when a statistically significant, dose-responsive, toxicologically relevant increase in the number of micronucleated polychromatic erythrocytes was observed for either the 24 or 48-hour kill times when compared to the vehicle control group.
If these criteria were not fulfilled, then the test item would be considered non-genotoxic under the conditions of the test.
A positive response for bone marrow toxicity would be demonstrated when the dose group mean polychromatic to normochromatic ratio was shown to be statistically significantly lower than the vehicle control group.
All data were statistically analysed using appropriate statistical methods as recommended by the UKEMS Sub-committee on Guidelines for Mutagenicity Testing Report, Part III (1989). The data was analysed following a √(x +1) transformation using Student's t-test (two tailed) and any significant results were confirmed using the one way analysis of variance.
no effects
Negative controls validity:
not valid
RESULTS OF RANGE-FINDING STUDY
- Dose range: 500 to 2000 mg/kg
- Clinical signs of toxicity in test animals: In animals dosed with the test item at 2000 mg/kg via the oral route, clinical signs were not observed in any of the animals. Therefore, with no evidence of toxicity the intraperitoneal route of administration was investigated to maximise exposure of the test item. Using the intraperitoneal route, the clinical signs hunched posture, ptosis, increased activity, and irritation and over grooming of the injection site were observed in animals dosed with the test item at and above 1000 mg/kg.
- Evidence of cytotoxicity in tissue analyzed: No
- High dose with and without activation: There was no mutagenic response in the highest dose group either with or without metabolic activation.
RESULTS OF DEFINITIVE STUDY
- Induction of micronuclei (for Micronucleus assay):The test item was found not to produce a toxicologically significant increase in the frequency of micronuclei in polychromatic erythrocytes of mice under the conditions of the test.
- Ratio of PCE/NCE (for Micronucleus assay): Statistically significant decreases in the PCE/NCE ratio were not observed in any of the test item dose groups when compared to the vehicle control group. However, the observation of clinical signs was taken to indicate that systemic absorption had occurred and exposure to the target tissue had been achieved.
- Statistical evaluation: There was no evidence of any statistically significant increases in the incidence of micronucleated polychromatic erythrocytes in animals dosed with the test item when compared to the vehicle control group.
There was no evidence of any statistically significant increases in the incidence of micronucleated polychromatic erythrocytes in animals dosed with the test item when compared to the vehicle control group.
The positive control group showed a marked increase in the incidence of micronucleated polychromatic erythrocytes hence confirming the sensitivity of the system to the known mutagenic activity of cyclophosphamide under the conditions of the test.
Mortality Data and Clinical Observations:
There were no premature deaths seen in any of the dose groups in the main test. Clinical signs were observed in animals dosed with the test item at and above 1000 mg/kg in both the 24 and 48-hour dose groups, where applicable, and included hunched posture and ptosis.
Summary of group mean data
Treatment group
Number of PCE with micronuclei per 2000 PCE
PCE/NCE Ratio
Group mean
Vehicle control (PBS) 10 ml/kg
24-h sampling time
Positive control (Cyclophosphamide) 50 mg/kg
23.0***
Sodium glucoheptonate 2000 mg/kg
Sodium glucoheptonate 500 mg/kg
PCE = Polychromatic erythrocytes
NCE = Normochromatic erythrocytes
SD = Standard deviation
*** = P < 0.001
Interpretation of results (migrated information): negative
The test item was considered to be non-mutagenic under the conditions of the test.
The study was performed to assess the potential of the test item to produce damage to chromosomes or aneuploidy when administered to mice. The method was designed to be compatible with the 1997 OECD Guidelines for Testing of Chemicals No.474 "Mammalian Erythrocyte Micronucleus Test", Method B12 of Commission Regulation (EC) No. 440/2008 of 30 May 2008, the US EPA (TSCA) OPPTS 870.5395, EPA 712-C-98-226, August 1998 guidelines, and be acceptable to the Japanese METI/MHLW/MAFF guidelines for testing of new chemical substances.
A range-finding test was performed to find suitable dose levels of the test item, route of administration, and to investigate if there was a marked difference in toxic response between the sexes. There was no marked difference in toxicity of the test item between the sexes; therefore the main test was performed using only male mice. Following discussions with the Sponsor, the micronucleus test was conducted using the intraperitoneal route in groups of seven mice (males) at the maximum recommended dose (MRD) of 2000 mg/kg and with 1000 and 500 mg/kg as the two lower dose levels. Animals were killed 24 or 48 hours later, the bone marrow extracted, and smear preparations made and stained. Polychromatic (PCE) and normochromatic (NCE) erythrocytes were scored for the presence of micronuclei.
Additional groups of mice were given a single intraperitoneal dose of phosphate buffered saline (PBS) (7 male mice) or dosed orally with cyclophosphamide (5 male mice), to serve as vehicle and positive controls respectively. Vehicle and positive control animals were killed after 24 hours.
There were no premature deaths seen in any of the dose groups in the main test. Clinical signs were observed in animals dosed with the test item at and above 1000 mg/kg in both the 24 and 48-hour dose groups, where applicable, and included hunched posture and included hunched posture and ptosis.
Statistically significant decreases in the PCE/NCE ratio were not observed in any of the test item dose groups when compared to the vehicle control group. However, the observation of clinical signs was taken to indicate that systemic absorption had occurred and exposure to the target tissue had been achieved.
The test item was found not to produce a toxicologically significant increase in the frequency of micronuclei in polychromatic erythrocytes of mice under the conditions of the test.
Based on the data available no classification for genotoxicity is needed according to GHS.

redpajama_set_name: RedPajamaCommonCrawl


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text:
Q: Using Django-tables2 with class-based view and non-default database throws "NameError: name 'TypeError' is not defined" I am trying to set up django-tables2 and followed the recommendations in their docs. However, if I call the view, it throws the error
File "/home/ubuntu/mysite/mysite_venv/lib/python3.8/site-packages/asgiref/local.py", line 94, in __del__
NameError: name 'TypeError' is not defined

Note: From what I could gather, this error message unfortunately also occurs in other contexts as the most upvoted thread deals with an Apache config problem. I would be glad to adjust the title for clarity once the issue has been grasped concisely.
Django-tables2 should access (read-only) a legacy MySQL database which I added behind the default SQLite database in settings.py (see further down).
My polls/models.py:
from django.db import models
import datetime
from django.db import models
from django.utils import timezone

...

class Dashboard(models.Model):
    host = models.CharField(db_column='Host', max_length=255, blank=True, null=True)
    title = models.TextField(db_column='Title', blank=True, null=True)
    operation = models.CharField(db_column='Operation', max_length=255, blank=True, null=True)
    performedat = models.DateTimeField(db_column='PerformedAt', blank=True, null=True)

    class Meta:
        managed = False
        db_table = 'dashboard'

In case it's necessary, the underlying table in MySQL looks like this:
c.execute('''CREATE TABLE dashboard(
            id INT PRIMARY KEY AUTO_INCREMENT,
            Host VARCHAR(255),
            Title TEXT,
            Operation VARCHAR(255),
            PerformedAt DATETIME);''')

My polls/views.py:
from django.shortcuts import render
from django.views.generic.list import ListView
from .models import Dashboard
from django.http import HttpResponse

class DashboardListView(ListView):
    model = Dashboard
    template_name = 'polls/dashboard.html'

Note: I have made sure that dashboard.html does reside in mysite/polls/templates/polls.
My polls/urls.py:
from django.urls import path

from polls.views import DashboardListView, detail, accept, reject

urlpatterns = [
    # ex: /polls/
    path('', DashboardListView.as_view()),
    #ex: /polls/5/
    path('<int:question_id>/', detail, name='detail'),
    #ex: /polls/5/accept/
    path('<int:question_id>/accept/', accept, name='results'),
    # ex: /polls/5/deny/
    path('<int:question_id>/deny/', reject, name='reject'),
]

My polls/dbrouters.py:
from polls.models import Dashboard

class DashboardDBRouter:
    def db_for_read (self, model, **hints):
        if (model == Dashboard):
            # your model name as in settings.py/DATABASES
            return 'dashbaord'
        return None

My dashboard.html (just used the tutorial template):
{# polls/templates/polls/dashboard.html #}
{% load render_table from django_tables2 %}
<!doctype html>
<html>
    <head>
        <title>List of persons</title>
    </head>
    <body>
        {% render_table object_list %}
    </body>
</html>

My settings.py:
# Application definition

INSTALLED_APPS = [
    'polls.apps.PollsConfig',
    'django.contrib.admin',
    'django.contrib.auth',
    'django.contrib.contenttypes',
    'django.contrib.sessions',
    'django.contrib.messages',
    'django.contrib.staticfiles',
    'django_tables2',
]

DATABASE_ROUTERS = (
    'polls.dbrouters.DashboardDBRouter',
)

...

TEMPLATES = [
    {
        'BACKEND': 'django.template.backends.django.DjangoTemplates',
        'DIRS': [],
        'APP_DIRS': True,
        'OPTIONS': {
            'context_processors': [
                'django.template.context_processors.debug',
                'django.template.context_processors.request',
                'django.contrib.auth.context_processors.auth',
                'django.contrib.messages.context_processors.messages',
            ],
        },
    },
]

...

DATABASES = {
    'default': {
        'ENGINE': 'django.db.backends.sqlite3',
        'NAME': BASE_DIR / 'db.sqlite3',
    },
    'dashboard': {
        'ENGINE': 'django.db.backends.mysql',
        'NAME': 'testdatabase',
        'USER': 'my_username',
        'PASSWORD': 'my_password',
        'HOST': 'my_host',
        'PORT': '3306'
    },
}

What I noticed is that if I open a shell with python manage.py shell and just call the manager via Dashboard.objects.all() I get
django.utils.connection.ConnectionDoesNotExist: The connection 'dashbaord' doesn't exist.

While if I call Dashboard.objects.all().using('dashboard') it seems to work since I then get
<QuerySet [<Dashboard: Dashboard object (1)>]>

Is it possible that something is wrong with my router? I thought it should connect automatically if I understood this answer correctly.
My second guess: I don't have much experience with Django and class-based views yet, so this might be completely off, but I am confused that neither my model nor my view contain any statements that contain any return or str() statements although I have found contrary examples here and here.
I thought that this might be the issue because it could explain the error in the sense that the Python interpreter is destroyed before the process is completed because nothing is returned as was discussed here (unfortunately without a clear result).
I honestly don't know where to go from here, any help is really appreciated.

A: There's a typo in your spelling of dashbaord (should be dashboard) in routers.py:
django.utils.connection.ConnectionDoesNotExist:
   The connection 'dashbaord' doesn't exist.
                  ^^^^^^^^^^^

redpajama_set_name: RedPajamaStackExchange


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