This site uses cookies.
Some of these cookies are essential to the operation of the site,
while others help to improve your experience by providing insights into how the site is being used.
For more information, please see the ProZ.com privacy policy.
This person has a SecurePRO™ card. Because this person is not a ProZ.com Plus subscriber, to view his or her SecurePRO™ card you must be a ProZ.com Business member or Plus subscriber.
Affiliations
This person is not affiliated with any business or Blue Board record at ProZ.com.
Services
Translation
Expertise
Specializes in:
Metallurgy / Casting
Medical (general)
Materials (Plastics, Ceramics, etc.)
Construction / Civil Engineering
Petroleum Eng/Sci
Science (general)
Also works in:
Engineering (general)
Business/Commerce (general)
Engineering: Industrial
Law: Contract(s)
Manufacturing
Nutrition
Finance (general)
Mechanics / Mech Engineering
Medical: Health Care
Medical: Instruments
Patents
More
Less
Rates
Portfolio
Sample translations submitted: 3
English to Chinese: Medical
Source text - English 1
Diet Causes Viral Mutation in Mice
A benign coxsackievirus can mutate and become virulent if its host, a mouse in this case, lacks the trace mineral selenium, researchers have discovered. Moreover, the altered virus can cause disease when it enters well-fed animals.
“This interesting work is the first to show that a nutritional deficiency can accelerate evolution of a virus population from benign to virulent in an intact animal,” assert Charles J. Gauntt of the University of Texas Health Science Center in San Antonio and Steven Tracy of the University of Nebraska Medical Center in Omaha. Their comments appear in an editorial that accompanies the announcement in the May NATURE MEDICINE of the findings by Melinda A. Beck of the University of North Carolina at Chapel Hill and her colleagues.
Coxsackieviruses infect more than 20 million people annually in the United States and can cause illnesses ranging from a cold to an inflammation of the heart. However, most of the viruses are benign, so only about 10,000 infected people become ill.
In previous studies, Beck and other researchers had linked coxsackievirus and heart disease to selenium intake in humans as well as mice. People deficient in the mineral tend to develop Keshan disease, an inflammatory heart disease. Scientists had found coxsackieviruses in Keshan patients, they note.
Last year, Beck and her colleagues reported their first inkling that the coxsackievirus mutates in nutritionally deprived hosts. The team found that a normally benign strain of coxsackievirus B3 (CVB3) damaged the hearts of selenium-deficient mice. Injecting virus from these animals into selenium-rich mice caused the healthy creatures to develop heart disease.
In their new study, Beck and her coworkers fed mice either a diet very low in selenium or a normal diet for 4 weeks, then injected benign CVB3 into both groups. After 7, 10, and 14 days, the scientists killed and examined 10 mice from each group. After only 7 days, the mice that lacked selenium showed signs of heart disease, including inflammation. The well-nourished mice stayed diseasefree.
The researchers compared the original virus, the virus taken from the hearts of the selenium- deficient mice, and strains of CVB3 known to cause heart disease. In the deprived mice, the original virus’ sequence of nucleotides, the building blocks of ribonucleic acid (RNA), underwent six changes. These same mutations appear in the CVB3 strain that causes heart disease, Beck and her colleagues report.
They speculate that the virus changes rapidly in selenium-deficient hosts because of the animals’ weakened immune systems. The mineral, an antioxidant, helps protect the immune system from the damaging by-products of normal metabolic functions. Also, coxsackieviruses and similar viruses mutate readily. Whether the virus requires all six or only one or two of the mutations to become virulent remains unclear, the authors note. They are now investigating why the changes occur at such specific sites on the genome and what happens to the virus in animals only slightly low on selenium.
If coxsackieviruses and other viruses become virulent when they infect nutritionally deprived people, that may “help explain the steady emergence of new strains of influenza virus in China, which has widespread selenium-deficient areas,” Beck’s team argues.
Our findings might even help to explain the crossing over of certain viruses [such as HIV] to a new host species through accelerated mutation rates,” the authors speculate. HIV apparently first infected monkeys and then moved to some humans living in selenium-poor regions of Africa, they note.
2
Antioxidants and Viral Infections: Host Immune Response and Viral Pathogenicity
Melinda A. Beck, PhD
Departments of Pediatrics and Nutrition, University of North Carolina
ABSTRACT
Malnutrition has long been associated with increased susceptibility to infectious disease. The increase in severity from and susceptibility to infectious disease in malnourished hosts is thought to be the result of an impaired immune response. For example, malnutrition could influence the immune response by inducing a less effective ability to manage the challenge of an infectious disease. Work in our laboratory has demonstrated that not only is the host affected by the nutritional deficiency, but the invading pathogen is as well. Using a deficiency in selenium (Se) as a model system, mice deficient in Se were more susceptible to infection with coxsackievirus, as well as with influenza virus. Se-deficient mice develop myocarditis when infected with a normally benign strain of coxsackievirus. They also develop severe pneumonitis when infected with a mild strain of influenza virus. The immune system was altered in the Se-deficient animals, as was the viral pathogen itself. Sequencing of viral isolates recovered from Se-deficient mice demonstrated mutations in the viral genome of both coxsackievirus and influenza virus. These changes in the viral genome are associated with the increased pathogenesis of the virus. The antioxidant selenoenzyme, glutathione peroxidase-1, was found to be critically important, as glutathione peroxidase knockout mice developed myocarditis, similar to the Se-deficient mice, when infected with the benign strain of myocarditis. This work points to the importance of host nutrition in not only optimizing the host immune response, but also in preventing viral mutations which could increase the viral pathogenicity.
Key words: influenza virus, coxsackievirus, selenium, glutathione peroxidase
Key teaching points:
• A deficiency in selenium and/or a deficiency in selenoenzyme glutathione peroxidase leads to increased susceptibility to coxsackievirus-induced myocarditis.
• A deficiency in selenium leads to increased susceptibility to influenza virus-induced pneumonitis.
• Increased virulence of coxsackievirus and influenza virus in Se-deficient hosts is due to changes in the viral genome.
INTRODUCTION
It has been known for many years that nutritional deficiencies can lead to increased susceptibility to infectious diseases [1,2]. Many viral infections, for example infections with rotavirus, measles, and parainfluenza virus, are much more severe in malnourished hosts as compared with well-nourished hosts. A well-known example is the association of vitamin A deficiency with the development of severe measles infections, leading to a high rate of mortality [3]. Indeed, vitamin A supplementation is recommended as a treatment for severe measles infection and supplementation with vitamin A is suggested at the time of vaccination for measles infection.
The association of poor host nutritional status with increased susceptibility to infectious disease has long been thought to be related to the host immune response. Thus, a host nutritional deficiency would lead to an impaired immune response. This impairment in immune function would result in increased vulnerability to infectious disease. Both general malnutrition, as well as specific nutritional deficiencies, have been reported to be associated with immune dysfunction, including impaired antibody responses, decreased macrophage activity and T cell dysfunction [4,5].
Although the immune response has been demonstrated to be impaired in nutritionally deficient hosts, our laboratory has also shown that the viral pathogen itself may be affected by the nutritional deficiency. Several viruses have been shown to develop increased virulence due to changes in their genomes as a result of replicating in a nutritionally deficient host. The mechanism for the viral genomic changes is not well understood, although it appears to be related to increased oxidative stress in the deficient host. Thus, both the host as well as the pathogen can be influenced by the nutritional status of the host.
KESHAN DISEASE, SELENIUM DEFICIENCY AND COXSACKIEVIRUS
Selenium (Se) is a trace mineral that is an essential component of a number of proteins, including glutathione peroxidase, glutathione reductase and thioredoxin reductase [5]. Se is believed to play an essential role in antioxidant protection due to its incorporation as selenocysteine into several antioxidant enzymes.
A deficiency of Se in China was found to lead to a cardiomyopathy known as Keshan disease [6]. Specific regions in China have Se-deficient soils and thus grains grown in the deficient soil are also deficient in Se. Individuals living in areas with Se-deficient soils who consume locally grown food will develop a deficiency in Se. Keshan disease is a cardiomyopathy characterized by necrotic lesions throughout the myocardium with varying degrees of cellular infiltration and calcification [7]. Supplying people living in Keshan disease endemic areas with selenium can prevent the disease.
However, the deficiency in Se did not appear to entirely explain the epidemiological pattern of the disease. Keshan disease had a seasonal and annual incidence, and not everyone who was Se deficient developed the disease. For these reasons, scientists in China suspected an infectious co-factor was required along with the deficiency in Se for the development of Keshan disease. Using both blood and tissue samples from Keshan disease victims, scientists in China were able to isolate enteroviruses from some of the samples [8]. Coxsackie B viruses were the most commonly identified.
Coxsackieviruses, small RNA enteroviruses in the Picornaviridae, are known to infect the heart and can cause myocarditis, or inflammatory heart disease. Using the technique of RT-PCR, several groups have reported coxsackievirus B3 sequences from archived Keshan disease hearts [9]. Thus, it appeared that a deficiency in Se together with a coxsackievirus infection resulted in Keshan disease.
In order to further characterize the relationship between infection with coxsackievirus and a deficiency in Se, a mouse model was used. Mice are well-established models for coxsackievirus-induced myocarditis and develop a pattern of heart inflammation similar to that found in humans. In addition, well-characterized strains of coxsackievirus, both myocarditic and amyocarditic in mice, are available.
Mice were fed a diet deficient in Se beginning at the time of weaning. After a period of 4 weeks, glutathione peroxidase activity, a marker of Se status, was 1/5 of the activity of glutathione peroxidase from Se-adequate mice. Thus, short term feeding of a Se-deficient diet led to a moderate deficiency in Se.
Se-deficient and Se-adequate mice were infected with a normally amyocarditic strain of coxsackievirus B3 (CVB3/0). At various times post infection, the mice were killed and tissues were removed for study. As expected, the Se-adequate mice did not develop myocarditis when infected with the amyocarditic strain of virus. However, the Se-deficient animals did develop a moderate level of myocarditis [10]. The myocarditis was characterized by inflammatory foci scattered throughout the myocardium.
Heart virus titers revealed that the Se-deficient mice had 10 to 100-fold higher levels of virus in the heart post infection compared with the Se-adequate mice. This result suggested that there was impairment in the immune response, such that the virus was not as controlled in the Se-deficient mice as in the Se-adequate mice. Interestingly, the deficiency in Se did not affect the timing of clearance, as both Se-adequate and Se-deficient mice cleared the virus from the heart by day 14 post infection.
The immune response of the Se-deficient mice was found to be altered. Although the production of neutralizing antibody responses was not affected, the proliferative response of T cells to both mitogen and antigen were decreased. Because inflammation is the hallmark of coxsackievirus-induced myocarditis, expression of mRNA for several inflammatory chemokines was examined [11]. Monocyte chemotactic protein-1 (MCP-1) was highly expressed at day 10 in the Se-deficient animals as compared with the Se-adequate animals. This increase in MCP-1 mRNA expression may be responsible for the inflammation found in the infected Se-deficient mice.
In addition to alterations in the expression of MCP-1 for MCP-1, expression of mRNA for -interferon (IFN) was greatly decreased in the Se-deficient mice [11]. -IFN is important in protecting cells from viral infection, and a decrease in -IFN may have been related to the increase in viral titers in the Se-deficient animals.
Thus, it appeared that an altered immune response might have been responsible for the myocarditis that developed in the Se-deficient mice infected with an amyocarditic strain of CVB3. Alternatively, the viral pathogen was also exposed to a Se-deficient environment and might also be affected.
COXSACKIEVIRUS GENOME CHANGES IN SE-DEFICIENT MICE
To determine if host factors alone were responsible for the development of myocarditis in the Se-deficient CVB3/0 infected mice, a passage experiment was performed. Se-adequate and Se-deficient mice were infected with CVB3/0. Seven days later, their hearts were removed and the virus isolated. The virus was renamed to reflect the tissue from which it had been isolated (CVB3/0Se+ isolated from Se-adequate animals and CVB3/0Se- isolated from Se-deficient animals). CVB3/0Se+ and CVB3/0Se- were passed back into Se-adequate mice. If the induction of myocarditis was due solely to host conditions, then the Se-adequate mice should not develop myocarditis from infection with either CVB3/0Se+ or CVB3/0Se-. However, Se-adequate mice infected with CVB3/0Se- developed myocarditis, whereas Se-adequate mice infected with CVB3/0Se+ did not. These results strongly suggested that the virus that replicated in the Se-deficient mice underwent a genomic change.
To confirm that a change in viral genome had occurred, viruses recovered from Se-adequate and Se-deficient mice were sequenced [12]. The sequence of CVB3/0Se+ (recovered from Se-adequate mice) was identical to the original stock virus used to inoculate the mice. However, the sequence of CVB3/0Se- (recovered from Se-deficient mice) had 6 point mutations. Each of the 6 mutations was also found in myocarditic strains of CVB3 virus. Thus, replication of CVB3/0 in a Se-deficient host leads to an alteration in viral genotype, changing a normally avirulent virus into a virulent one due to point mutations in the viral genome.
GLUTATHIONE PEROXIDASE AND COXSACKIEVIRUS
Why would a deficiency in Se lead to a change in viral genotype? One possibility is the association of Se with antioxidant enzymes. In particular, glutathione peroxidase, of which there are 4 isozymes, is a major component of the cellular antioxidant system. A deficiency in Se leads to a decrease in glutathione peroxidase activity. To determine if the decrease in glutathione peroxidase activity was associated with the increase in susceptibility to CVB3/0 induced myocarditis of Se-deficient mice, glutathione peroxidase-1 knockout mice were utilized.
Glutathione peroxidase-1 (GPX-1) knockout mice develop normally and do not have compensatory increases in other antioxidant enzymes under normal conditions [13]. However, GPX-1 knockout mice are at a higher risk for mortality when exposed to the pro-oxidant compound paraquat [14]. When infected with CVB3/0, a little over half of the GPX-1 knockout mice develop myocarditis, whereas CVB3/0 infection of wildtype mice does not induced myocarditis [15]. These results suggested that the increased susceptibility of Se-deficient mice to develop myocarditis when infected with CVB3/0 was associated with a decrease in the activity of GPX-1.
The immune response of the GPX-1 KO mice was also altered in response to infection with CVB3/0. Neutralizing antibody levels were greatly decreased in the GPX-1 KO mice as compared with wildtype mice, although T cell proliferative responses to both mitogen and antigen were not affected. These results are in contrast to the results from the CVB3/0 infected Se-deficient mice, in which T cell proliferative responses were greatly inhibited and no changes in the production of neutralizing antibody were noted.
Cardiac viral titers were equivalent between CVB3/0 infected GPX-1 KO mice and wildtype mice. This was in contrast to Se-deficient mice, which developed higher cardiac titers when compared with Se-adequate mice. As was found for Se-adequate and Se-deficient mice, both wildtype and GPX-1 KO mice cleared virus from the heart at an identical rate.
Sequencing of virus recovered from CVB3/0 infected GPX-1 KO that developed myocarditis revealed seven nucleotide changes when compared with the stock virus [15]. Virus recovered from the infected wildtype mice had no genome changes when compared with stock virus. Six of the seven nucleotide changes found in virus recovered from GPX-1 KO mice were identical to the changes found in Se-deficient mice. Of particular importance, genomic changes were found only in virus recovered from CVB3/0 infected GPX-1 KO mice that developed pathology. The sequence of the CVB3/0 virus isolated from infected GPX-1 KO mice that did not develop cardiac pathology was identical to the stock virus. Thus, changes in the viral genome were responsible for the development of myocarditis in the GPX-1 KO mice.
INFLUENZA VIRUS AND SE-DEFICIENCY
Clearly, replication of coxsackievirus in a Se-deficient host leads to changes in the viral genome. Once these genomic changes occur, even mice with normal nutriture are susceptible to the newly pathogenic strain of virus. To determine if viruses other than coxsackievirus were also susceptible to changes in the viral genome due to replication in a Se-deficient host, infection with influenza virus was studied.
Influenza virus is a segmented RNA virus in the Orthomyxoviridae family. These viruses are responsible for a great deal of morbidity and mortality each year. Older adults and those with chronic diseases of the lung and/or heart are at the highest risk of dying from an influenza virus infection. Influenza viruses have a propensity to alter their surface proteins in order to escape early detection by the immune system of an infected host [16]. One such process is known as antigenic drift and is responsible for new strains of influenza that arise each year and infect their newly susceptible hosts due to small changes in the hemagluttinin (HA) and neurominidase (NA) proteins, both of which are exposed on the viral surface. The HA and NA are recognized by the host antibody response, and changes in these two proteins can lead to the ability of the virus to escape immune detection. In addition, large-scale changes in the influenza virus surface proteins due to reassortment of viral RNA segments between influenza strains are also possible. Known as genetic shift, these large changes in the viral genome are responsible for worldwide pandemics that have occurred several times throughout history.
To determine if a deficiency in Se would affect the pathogenicity of an influenza virus, Se-deficient and Se-adequate mice were infected with a mild strain of influenza, influenza A/Bangkok/1/29. At various times post infection, the mice were killed and the tissues harvested. Se-deficient mice developed much more severe lung inflammation post influenza infection when compared with the infected Se-adequate mice [17]. The infiltrate in the lungs of the infected mice consisted predominantly of macrophages, CD4+ and CD8+ T cells. Se-deficient mice had decreased percentages of CD8+ cells infiltrating the lungs, compared with Se-adequate mice.
Examination of draining lymph nodes for mRNA for a variety of cytokines and chemokines revealed that infected Se-deficient mice had an increase in the production of pro-inflammatory cytokines and chemokines. In addition, the type of cytokine production was TH2-like (pro-inflammatory) as opposed to the more TH1-like pattern found in infected Se-adequate animals.
Sequencing of the mRNA segments that code for viral surface proteins (HA-hemagluttinin and NA-neurominidase) revealed little difference between virus recovered from Se-deficient vs. Se-adequate animals. However, the mRNA that codes for the matrix protein revealed 29 nucleotide changes, of which six led to amino acid changes. Virus recovered from Se-adequate animals had two nucleotide changes, of which one led to an amino acid change [18].
This finding was unexpected, as the matrix protein is relatively stable and exhibits little change among influenza virus strains. One possible explanation is that the matrix protein is internal, and thus not subjected to immune pressure from the host antibody response. In contrast, changes in the HA and NA proteins are responsible for the ability of the virus to escape detection by a previously exposed host. The HA and NA are exposed on the surface of the virion and are therefore exposed to immune pressure.
To date, we have sequenced only three of the eight RNA segments of the influenza virus. Although we found many more changes in the matrix protein of the virus recovered from Se-deficient mice as compared with virus recovered from Se-adequate mice, we do not know if other changes are present in the influenza virus genome. Further investigation is currently underway.
CONCLUSIONS
Studies utilizing both Se-deficient mice as well as GPX-1 knockout mice demonstrate both Se and GPX-1 activity as providing a unique role in preventing enhanced virulence of both coxsackievirus as well as influenza virus. As diagramed in Fig. 1, in addition to having an effect on the immune system of the host, a deficiency in Se and/or a deficiency in glutathione peroxidase activity can lead to enhanced virulence of a viral pathogen due to genetic changes in the viral pathogen itself. Once these changes have occurred, even hosts with normal Se status and glutathione peroxidase activity are susceptible to its newly virulent properties.
Fig.1. Diagram depicting the influence of a lack of selenium or glutathione peroxidase activity on the development of pathogenesis post viral infection.
This work suggests a new way of examining the effect of host nutritional deficiencies on increased susceptibility to viral infection. Although it is clear that nutritional deficiencies can have a profound effect on host immunity, as shown by us as well as many others, it is also clear that the viral pathogen itself is susceptible to the deficiency.
What is the mechanism that allows the viral pathogen to mutate in the deficient host? One possibility is a selection mechanism. Both coxsackievirus and influenza virus are RNA viruses which have a high mutation rate due to a lack of proofreading enzymes during replication. Thus, mutant viruses will be generated each time the virus replicates and sequencing of the virus reveals only the consensus or dominant sequence. A host deficiency in Se leads to alterations in the immune response of the infected host, which in turn could allow the selection of a new viral variant with more pathogenic properties. A second possibility may involve increased oxidative stress that occurs in the Se-deficient mice due to a lack of the antioxidant glutathione peroxidase. The increased oxidative stress status of the host may cause direct damage to the viral RNA itself, resulting in new mutations that lead to enhanced pathogenesis. Both of these possibilities are currently under investigation.
In summary, the nutritional status of the host is an important variable when considering viral pathogenesis. With the current interest in emerging infectious diseases, it would be important to consider the host nutritional status as a driving force for viral mutations.
Translation - Chinese 1
饮食在小鼠中引起的病毒突变
研究人员发现，如果宿主，例如小鼠缺少微量元素矿物硒，良性柯萨奇病毒就可能突变，成为恶性病毒。此外发生了变化的病毒，如果进入饲养良好的动物，就可引起动物发病。
驻San Antonio的Texas大学健康科学中心的Charles J. Gauntt和驻Omaha的Nebraska大学医疗中心的Steven Tracy声称“这项很有趣的工作首次表明健康的动物如果缺少营养，体内的良性病毒就可快速变成恶性病毒。”
柯萨奇病毒在美国使两千多万人受到感染，引起的疾病从感冒到心脏发炎。不过，大多数病毒是良性的，受感染的人得病的只有一万多人。
在过去的研究中，Beck和她的同事们将柯萨奇病毒和心脏病与人类和小鼠硒的摄取量联系起来。人们如果矿物质就会患克山病，克山病是一种炎性心脏病。
去年，Beck和她的同事们报告称，他们模糊地认识到柯萨奇病毒在缺乏营养的宿主中突变。他们发现，通常是阳性的柯萨奇病毒B3 (CVB3)菌株会损害缺硒小鼠的心脏。把这些动物中的病毒注射到富硒小鼠中，这些健康的小动物也会患上心脏病。
Beck和她的同事们在最新的研究中把小鼠分成两个小组，用硒含量很低的和正常的食物喂养4周时间，然后注射良性CVB3，分别在7，10和14天后屠杀和检测每个小组的10只小鼠。在7天后屠杀的小鼠中，只有缺硒的小鼠表现又患心脏病的迹象，营养良好的小鼠没有得病。
研究人员对原病毒进行了比较，其中包括从缺硒小鼠的心脏中获取的病毒和已知导致心脏病的CVB3菌株。在得病的小鼠中，原始病毒的核苷酸顺序和核糖核酸建筑块发生了6种变化。在导致心脏病的CVB3菌株中也出现了同样的突变。
他们设想，缺硒宿主发生的病毒快速变化是由于动物的免疫系统降低。矿物质是一种抗氧化剂，有助于防止免疫系统遭受正常代谢功能副产品的损害。此外，柯萨奇病毒和与之相类似的病毒突变很快。
Beck等人争辩说，如果柯萨奇病毒和其他病毒在感染了营养不良的人群后变成毒型病毒，这可“有助于对在中国不断出现的流感病毒新菌株做出解释，中国有很多地方缺硒。”
作者们认为，“我们的发现甚至有助于解释为什么有些病毒，例如艾滋病病毒会通过加速突变传染给新宿主物种。”艾滋病病毒显然是先感染猴子，然后在传染给生活在缺硒地区的人群。
Source text - English 5
Forging
The Present and Future of Forging Simulation
Computer programs can predict die fill, load, energy, and defect formation. As applications advance and technology matures, simulation will continue to evolve into a daily production activity, even at the smallest forge shops.
Initially, forging simulation software was used by a small group of companies in the U.S. in the 1980s. The Analysis of Large Plastic Incremental Deformation (ALPID) program was developed at the Battelle Memorial Institute under sponsorship by the U.S. Air Force to support the development of gas-turbine forgings, to be used in the Advanced Tactical Fighter and other USAF systems.
At the time, it was a challenge to set up a simulation with very primitive preprocessing tools, extended simulation times, minimum graphics, and technical problems. Realistically, one could expect to spend several days to run a typical turbine disk simulation; with quite a bit of manual intervention. Despite those early challenges, ALPID flourished at companies striving for any edge in a very competitive market.
While ALPID was successful as a project code, Battelle staff applied their experience and background to the development of DEFORM. ALPID was limited to two-dimensional (2D) simulation for axi-symmetric (round) parts due to computer speed and software limitations. Initial applications included optimizing billet and blocker design, die fill, forging loads, and defects.
One by one, companies adopted simulation as a critical element of the design process. In 1991, the former Battelle staff that developed both ALPID and DEFORM founded Scientific Forming Technologies Corp.. The barriers to forging simulation were significant. SFTC executive vice president and co-founder Dr. Wei-Tsu Wu recalls that “practical 3D simulation was unthinkable. Problems included computing speed, mesh generation, element performance, and user interface.”
Fast forward to today. Forging (see November/December 2005, p.16) reports that 80% of the large companies (250+ employees), 75% of the mid-sized companies (100-249), and even 50% of smaller firms (50-99) are using process simulation. These numbers have more than doubled over the last decade, similar to the expanded use of CAD systems in the early 1980s. Computer modeling has become an integral part of the design and development process not only at the leading organizations, but at most forging companies.
For those not familiar with the subject, forging simulation is a computer program used to predict die fill, load, energy, and defect formation. This is based on the fact that the workpiece flows to the path of least resistance when displaced by one or more dies. The load is based on the forging size, shape, friction, temperature, and material properties. With the die fill defined, simulation can directly calculate critical process information including strain, stress, and temperature. With maturity, the prediction of grain flow, shear banding, and fracture have evolved.
Typical forging applications
Simulation applications are widely published in conference journals, magazine articles, and marketing material by simulation suppliers. Examples of common applications include:
Defect prediction—During the quotation process, an aluminum component was simulated using DEFORM-3D to evaluate material flow and die fill. A piping defect was predicted prior to finalizing the quote (see Fig. 1). At that time, when little was committed, the supplier and customer were in a good position to discuss and consider alternatives. A trial of the original design confirmed the solution accuracy, as shown.
Product development—Competition and customer requirements have led to the development of more complex parts being produced to tighter tolerances, at a lower cost, and in less time. While most developments evolve over time, some are revolutionary. Ten years ago, helical gears for automobiles were machined from round forgings or bar stock. Today, high-volume gears are cold-extruded or hot-forged with gear teeth in a finished or nearly finished geometry. In these cases, process simulation (see Fig. 2) has been used extensively to develop the process, preform, and tooling.
Product optimization—The Forging Defense Manufacturing Consortium’s (FDMC) PRO-Fast Project, sponsored by the Defense Logistics Agency, has been documented in Forging.
One of its success stories involved a hammer forging of steel bomb lugs. This high-volume forging experienced a range of problems including die wear, forging laps, locating the buster in the blocker cavity, and an 11% scrap rate. DEFORM-3D was used to test ideas and designs from Delfasco, New Die (the toolmaker), and SFTC personnel. (see Fig. 3)
Simulation provided quantitative feedback on the influence of each idea. Studying total energy required to deform the part provided an indication of the number of hammer blows. Process stability could be determined by running multiple cases with slight variations in location. At the end of the day, the dies were changed to include roll, bust, block, and finish stations. Fewer hits in the roll station (and overall) were required. The scrap rate was reduced to 3% after 16,000 forgings (48,000 lugs). Simulation was integral to this process improvement.
Today’s simulation tools provide insight into and information about a design or process. Simulation does not design or develop the process. The mind of an experienced designer is still superior to any computer program for preform geometry, process development, and overall forging strategy.
Currently, simulation is used to provide critical information to improve the performance of the designer. As optimization techniques are developed, the contribution of simulation to the design details will continue to increase.
Advanced and future applications
While forging simulation continues to mature, software and applications are being developed at a rapid pace. A sampling of interesting developments include:
Heat-treatment simulation—A wide range of projects have contributed to the development of heat-treatment simulation. This is a far more challenging problem than forging simulation, due to complex material behavior at the microstructure level. Practical requirements include the prediction of mechanical properties and heat-treatment distortion. The image in Figure 4 shows the result of a DEFORM-HT simulation of a forged axle beam before (white) and after (yellow) heat treatment. Most of the volumetric change resulted from a phase transformation to martensite.
Machining distortion—Forming and heat-treatment operations induce internal stresses in metal components. These stresses come to equilibrium as the part distorts. Remaining stresses are called residual stress. When a part is machined, the internal stress balance is disturbed. Thus, a new equilibrium is established, resulting in part distortion. The image in Fig. 5 shows a turbine disk in the machined (yellow) state superimposed on the distorted part (orange). Several companies are running two-dimensional machining distortion simulations for turbine disk applications. Three-dimensional capabilities are under development.
Design optimization—A fully automated blocker design program has been envisioned by researchers for decades. To date, the human mind remains the best blocker design system. On the other hand, work is being done with sensitivity analysis, optimization, and other methodologies that will result in a workable system in the future.
In January/February 2000, Forging reported on the use of DEFORM-HT and iSIGHT to optimize heat-treatment processes in turbine disks. While this is an advanced application for the typical forge shop, industry leaders were using the technology for a decade or more. The article states, “Through the use of the program, residual stresses on the forged disks have been reduced by as much as 60%, and part distortion during subsequent machining has been reduced by as much as 30%. Such reductions have allowed every disk to meet machining tolerance.”
Industry changes
Simulation has been accompanied by cultural changes in the industry. Twenty-five years ago, very few designers or engineers even heard the term flow stress, effective (plastic) strain, or strain rate. Today, these are common terms.
The Forging Industry Assn. has recognized this important trend and responded by increasing simulation content in their Die Design and Press Design workshops. Initially, there was a one-hour lecture on this topic. Today, simulation examples are used throughout the courses.
Training of young engineers and designers has been influenced by simulation. The FDMC-sponsored Forging Fundamentals 101 was conducted prior to the 2005 Forging Industry Technical Conference. This workshop used simulation extensively to train attendees on the science behind forging. The cultural shift involves the ‘artisan’ methods of the past being supplemented, and in some cases replaced, by engineering and science.
Ease of use is not to be taken lightly. Researchers and analysts have used FEM codes for 25 years. Concepts such as element size, boundary conditions, convergence criteria, and time step are fairly routine. The forging market for simulation consists of designers and engineers that understand this very complex process through experience and intuition.
One challenge for code developers is to translate the user requirements into the FEM inputs. For example, SFTC released DEFORM-F3 in 2004. This three-dimensional program can be used easily by the designer or forging engineer. When setting up a forging simulation, there is a trade-off between speed and detail/accuracy. In DEFORM-F3, a slider bar was developed to automate the setup process based on the user requirement in very simple terms.
There are also a wide range of intermediate applications for forging simulation. Experienced users are modeling equipment interactions for hammers and presses, and analyzing die failures using die-stress analysis. They are comfortable with the science behind the process, and comfortable with advanced applications.
These advanced applications should be kept in perspective. Technically savvy analysts will find a way to take advantage of new capabilities as they are being developed. Designers with less modeling experience would be advised to start with proven applications. On the other hand, when selecting simulation software it can be useful to review the advanced applications to understand if it is on the leading edge of application development or in a catch-up mode.
In any case, simulation is useful in a wide range of production and development applications. Information is made available much faster than with shop trials or other experiments. Additionally, it is possible to visualize the process in a way that is not possible on a production forging press or hammer. As applications advance and technology matures, simulation will continue to evolve into a daily production activity, even at the smallest forge shops. Very few forge shops will succeed in the future without the effective use of process simulation.
Dr. Wu believes that within a decade, companies will model the surface condition, microstructure evolution, and microstructural properties. In fact, the limits may be related to material research and understanding.
Source text - English 1.
Characterization of Precipitates in Vanadium and Titanium Micro-alloyed Steels
Transmission electron microscopic observations were carried out on carbon extraction replicas prepared from two commercial V-microalloyed steels and one commercial Ti-microalloyed steel hot rolled to 10mm diameter bars at different rolling conditions.
The presence of about 0.13% Cu in V- or Ti-microalloyed steels led to the formation of copper sulphides preferentially rather than manganesesulphides although the steels containing more than 1% Mn. In Ti-microalloyed steel, globular titanium carbosulphides of the type Ti4C2S2 are observed in addition to copper sulphide.
In V-steels, transmission electron microscopy revealed very fine precipitates in the pro-eutectoid ferrite(≌5nm) which are identified as carbides or carbonitrides of the type M(C, N) (M=V and Cr, where V/Cr≌5). Some relatively coarse particles (≌0.1µm) were also observed (with V/Cr>15) which are suggested to be V-nitrides or carbonitrides formed at relatively high temperatures in austenite.
In Ti-steel, coarse titanium nittide particles (>5µm) were observed together with precipitates of the type MC(M=Ti and Cr) in the form of very fine precipitates(≌5nm, Ti/Cr≌9) or relatively coarse carbide particles (≌0.1µm. Ti/Cr>30).
1. Introduction
In recent years, successful improvement in the mechanical properties of low-carbon steels has been achieved by microadditions of strong carbide-forming elements such as niobium, vanadium or titanium. Such microalloyed steels have higher strength levels as a result of grain refinement of ferrite.The resulting fine-grained structure is often further strengthened by fine precipitates of particular alloy carbide. For strengthening ferrite the precipitate must be fine and for niobium steel, it has been estimated that formaximum strength the particle diameter should be about 3nm.1)
Precipitation strengthening has been examined in high Purity steels.2,3) However, no attention has been given to the effects of element present in the commercial steels such as copper and chromium on the precipitation behavior of V- or Ti-microalloyed steels. The present study presents the transmission electron microscopic observations carried out on commercial V- and Ti-microalloyed steels in the hot rolling condition.
……….
5. Conclusions
In hot rolled V- and Ti-microalloyed steels, transmission electron microscopy revealed several types of non-metallic inclusions and precipitates:
(1) Globular (0.2-1.0µm diameter) and elongated (up to lOµtm long) copper sulphides identified as CuS and Cu2S in vanadium and titanium microalloyed steels, respectively.
(2) Globular titanium carbosulphide Ti4C2S2 (0.2-0.5µm of diameter) and coarse cuboidal titanium nitride particles (5-lO µm side length) in Ti-microalloyed steel.
(3) Very fine precipitates in the pro-eutectoid ferrite (≌5nm) identified as carbides or carbonitrides of the type M(C,N) (M=V and Cr, where V/Cr ≌ 5) in V-steels and carbides of the type MC (M=Ti and Cr, where Ti/Cr ≌ 9) in Ti-steel.
(4) Relatively coarse (≌O.1µm) particles of V- nitrides or carbonitrides (with V/Cr>15) in V- microalloyed steels, and Ti-carbides (with Ti/Cr>30) in Ti-microalloyed steel.
2.
Influence of Heat Treatment on the Properties of Wear Resistant Tungsten Carbide Embedded Nickel Base Coating Produced by Gas Thermal Spray Process
The hard surfacing of mild steel substrate was carried out by thermal spraying of commercially available nickel base tungsten carbide powder under oxy-acetylene flame, The influence of pre and post spray heating on the morphology, hardness and wear characteristics of the coating were studied. The increase in preheating up to 400'C and post spray heating up to 900'C was found to enhance the hardness and wear resistance of the coating. However, the properties of the coating were found to vary across the coating showing a maximum hardness and wear resistance in the region some where in between its surface and the interface with the mild steel. The possibilities of occurring of various kinds of transformation during spraying as well as during post spray heat treatment have been analyzed as a cause of variation in distribution of property across the coating.
l. Introduction
The world wide attention on reclaimation of worn out metal parts and enhancement of wear life has been provoked the technologists to think for various type of hard surfacing of conventional material to a great extent. Depending upon service requirements various types of hard surfacing material has been used so far, where the process of hard surfacing such as the weld metal de-position, plasma spraying, thermal spraying etc, has been primarily decided on process economy and suitability of application to the components. Out of various hard surfacing processes the thermal powder spray technique has been found as a comparatively cheaper and versatile process. The hard surfacing materials are generally eutectic alloys based on cobalt, nickel, tungsten, chromium e/c. having dispersion of various types of carbides. Thus, during deposition of powder at high temperature the occurrence of various types of transformation in it is inevitable which, governs significantly the properties of the coating. Moreover, during deposition some kind of powders may form some metastable phases in the coating which may become stable by further transformation through a diffusion process under a post spray heat treatment and may provide a positive influence towards the wear resistance property of the coating. The utility of post spray heat treatment in improvement of the hardness of thermal spray coating has already been marked in an earlier work.1) However, sufficient work has not been reported so far to form a clear cut understanding in this direction, so that an effective post spray heat treatment can be designed for the coatings of various systems.
To develop a further understanding in this area an investigation has been carried out to study the influence of post spray heat treatment on the properties of a nickel base tungsten carbide dispersed coating produced on mild steel substrate by thermal spray of powder technique. In this work an effort has also been made to analyze the possibilities of occurring various kinds of transformations during the entire process affecting the characteristics of the coating.
…………
4. Conclusions
The post spray heating influences the hardness of the matrix and the embedded tungsten carbide particles by enhancing the same significantly. This improves the wear resistance of the coating to a great extent and provides a better life to the hard surface generated on the structural steel. However, a detail work should be carried out further to establish the Phenomena playing a significant role in transformation of various components of the coating under post spray heating.
3.
Enhancement of Resistance against Oxidation with Carbon Dioxide for Formed Coke and Electrode-grade Graphite and Carbon by Infiltrating Carbon into Pores
Formed coke, electrode-grade graphite (E.G,) and electrode-grade carbon (E.C.) were modified by infiltrating carbon within the pores by use of methane cracking. The rate of oxidation with CO. was lowered for all these samples but the amount of reduction was dependent on pore structures. Decrease in the rate for the electrode-grade carbon was very large compared to other samples. The mechanism of enhancement of resistance against oxidation was explained in terms of the pore structure changes accompanying infiltration and oxidation.
1. Introduction
The degradation of coke in a blast furnace is considered to be mainly due to decrease in mechanical strength accompanying the oxidation: C+ C02=2CO.1•2) Therefore, if low-grade coke which is generally sensitive to oxidation is improved by having its resistance to oxidation increased up to that of regular coke, it can be used in a blast furnace.
From this view point, modifications of low-grade coke have been tried to enhance the resistance to oxidation. Ogawa et al. used liquid tar to impregnate pores in coke.3) They reported an improvement of the mechanical ambient tumbler strength and also the mechanical strength after oxidation. However, a vast amount of soot produced prevented the application to a commercial process.4) Vandezande also reported on the infiltration of coke by use of hydrocarbons. However, he coated the outer surface of coke by deposited carbon.5) He also reported an improvement of mechanical ambient tumbler strength and also the mechanical strength after oxidation. However the effect was not so large because coke was oxidized at nearly the same rate after the outer surface layer of carbon was removed by oxidation. Therefore, these trials have not succeeded in being applied to a commercial process.
The present authors reported that the reactivity of the metallurgical coke with C02 could be lowered by infiltrating carbon into the pores where major oxidation occurs6) and that the mechanical strength after oxidation of the infiltrated coke increased greatly.7,8) For infiltration, methane cracking: CH4= C+2H2 Was used. In this case, the macropores are not necessary to be impregnated because the major oxidation is considered to occur in the small pores owing to their relatively larger specific surface area than that of macro- pores. This is very important factor in applying the technique to a commercial process because a short time for infiltration is desirable for the economics ofproduction.8)
In the present paper, formed coke was infiltrated and then oxidized in the same way as described in the previous paper.6) Formed coke is currently not exploited in a blast furnace because it has high reactivity to C02 in general and this is considered to be the major problem for formed coke.
Electrode-grade graphite (E.G.) and electrode-grade carbon (E.C)* were also tested to consider the effect of the difference in pore structure. The changes of pore size and surface area were determined by use of a mercury porosimeter.
…………
5. Conclusion
In order to modify the formed coke so as to have the higher oxidation resistance, carbon was infiltrated into pores using methane cracking. Impregnation of small pore or micropore is very important because oxidation occurs mainly in these pores where the specific surface area is far larger than that of macropores. In the previous paper,6) decrease in oxidation rate for the infiltrated metallurgical coke and an extreme increase in CSR(Coke Strength after C02 Reaction) of infiltrated metallurgicalcoke7,8) was shown.
As the formed coke has not been employed in a blast furnace and one of the reasons of it is the high reactivity to C02 for ordinary formed coke, we aimed at modifying it to have high resistance to oxidation by infiltrating carbon using methane cracking. In the present paper, as the main objective is to study how the enhancement of the resistance to oxidation is depending on the pore structures, carbonaceous materials having different pore structures: electrode-grade graphite (E.G.)and electrode-grade carbon (E.C.) were also used. The effect of infiltration was apparent for all these samples but the degree of decrease in oxidation was dependent on the pore structures. The results are summarized as follows:
(1)The oxidation rate of formed coke was lowered by infiltration and the rate decreased with increasing time. It became half of that of original formed coke 6ks after oxidation started. This reduction is considered to be caused as follows.
The infiltration occurred in both macropores (r=1-lOµm) and small pores (r
An associate professor of translation conferred by Hebei Provincial High-grade Translator Evaluation Committee in l990
A senior translator with over 40 years’ translation experiences and specialized in translation of technical materials about iron and steel making, casting, rolling and processing as well as glass manufacture and medicine
From 1985 to 1994, when I worked with Tangshan Iron and Steel Company, I translated nearly 100 articles from foreign magazines such as “Iron and steel engineer”, “I&SM”, “MPT”, “JSIJ International” and had them published in over 10 departmental and provincial journals including “Foreign iron and steel”, “Electric furnace”, “Continuous casting”, “Steel rolling”, “Welded pipe and tube” “Foreign refractory”, “Metallurgical industry automation”, “Industrial heating”, “International developments in metallurgy”, “Foreign coking chemistry”, “Fantai”, “Gangtie Fantai”, “Guowai Jinshu Rechuli”, “Shandong Yejin” and “Gansu Yejin”.
Since 1994, when I was retired in advance, I have been engaged successively by Tangshan Translation and Service Center, Qinhuangdao Translation and Service Company and Qinghuangdao Taiji Ring Nano-Product Com., Ltd and have worked as a part-time translator for Beijing Qinxihuayu Translation Company, Beijing Sagive Translation Company, Beijing Hongtenghuida Translation Company, Beijing Huaqing Translation Company, Shanghai Yes Meaning Translation Company, Guangzhou Tongwen Translation Company, Chengdu Huayi Translation Company and Yangzhou Yihai Translation Company. In this period, I have done a lot of translation in the fields of metallurgy, machinery, cement, refractory, glass, ceramics, papermaking, medicine, oil, chemistry, agriculture, husbandry, construction projects, economy, finance, foreign trade and others.
Keywords: Iron and steelmaking, casting, rolling, forging, glass, oil, petrochemical, civil construction, medical, contract. See more.Iron and steelmaking, casting, rolling, forging, glass, oil, petrochemical, civil construction, medical, contract, agreement, bidding, Articles of association, operation and maintenance instruction, manual,etc.. See less.
Expertise