• Journal of Korean Society of Industrial and Systems Engineering
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• v.16 no.27
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• pp.73-82
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• 1993

In this paper, We determine the expected travel time for several forks Storage/Retrieval machine which is allowed multiple stops in aisle. When throughput is increased, We propose adding to fork number of each S/R machine rather than adding to number of S/R machine, We also describe such a model which determines the optimal number of each several forks S/R machine subject to constraints on the hourly throughput and warehouse dimensions. Numerical example is presented to compare warehouse shapes against each single fork, twin forks, triple forks S/R machine for various throughput values.

• The Transactions of the Korea Information Processing Society
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• v.4 no.10
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• pp.2544-2552
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• 1997

This paper presents three multiprocess models for parallel protocol implementation, that is, (1)channel communication model, (2)fork-join model, and (3)event polling model. For the specification of parallelism for each model, a parallel programming language, Par. C System, is used. to measure the performance of multiprocess models, we implemented the Internet Protocol Suite(IPS) Internet Protocol (IP) for each model by writing the parallel language on the Transputer. After decomposing the IP functions into two parts, that is, the sending side and the receiving side, the parallelism in both sides is exploited in the form of Multiple Instruction Single Data (MISD). Three models are evaluated and compared on the basis of various run-time overheads, such as an event sending via channels in the parallel channel communication model, process creating in the fork-join model and context switching in the event polling model, at the sending side and the receiving side. The event polling model has lower processing delays as about 77% and 9% in comparison with the channel communication model and the fork-join model at the sending side, respectively. At the receiving side, the fork-join model has lower processing delays as about 55% and 107% in comparison with the channel communication model and the event polling model, respectively.

• The KIPS Transactions:PartA
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• v.10A no.4
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• pp.305-312
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• 2003

In the embedded Linux environments, developers can concurrently debug multiple processes that have parent-child relationships using multiple gdbs and gdbservers. But, it needs additional coding efforts and messy works of activating another gdbs and gdbservers for each created process, and so, it may be inefficient in the viewpoint of developers. In this paper, we propose a mgdb library and mgdbserver that supports concurrent debugging of multiple processes in the embedded Linux systems by using the library wrapping mechanism without modifying the kernel. Also, through the experimentation of concurrent debugging for multiple processes that communicate by an unnamed pipe, we show that our proposed debugging mechanism is more efficient than the preexisting mechanisms.

• The Journal of the Korea Contents Association
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• v.22 no.2
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• pp.71-79
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• 2022

Currently, even if control and mock hacking are performed for the security of web servers, vulnerabilities continue to occur and be hacked. To solve this problem, we have developed a secure web server that can control all web communication using sockets between L4 and L5. And when giving HTTP responses, we proposed a method of combining files and headers in advance. As a result, both security and speed could be improved. Therefore, in this paper, we proposed the reason why vulnerabilities occur even if control and mock hacking occur, a solution to it, and a security web server development method that can maintain security up to DB.

• Journal of Food Hygiene and Safety
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• v.22 no.1
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• pp.1-14
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• 2007

The term, "food safety", has traditionally been viewed as a practical science aimed at assuring the prevention acute illnesses caused by biological microorganisms, and only to a minor extent, chronic diseases cause by chronic low level exposures to natural and synthetic chemicals or pollutants. "food safety" meant to prevent microbiological agents/toxins in/on foods, due to contamination any where from "farm to Fork", from causing acute health effects, especially to the young, immune-compromised, genetically-predisposed and elderly. However, today a broader view must also include the fact that diet, perse (nutrients, vitamins/minerals, calories), as well as low level toxins and pollutant or supplemented synthetic chemicals, can alter gene expressions of stem/progenitor/terminally-differentiated cells, leading to chronic inflammation and other mal-functions that could lead to diseases such as cancer, diabetes, atherogenesis and possibly reproductive and neurological disorders. Understanding of the mechanisms by which natural or synthetic chemical toxins/toxicants, in/on food, interact with the pathogenesis of acute and chronic diseases, should lead to a "systems" approach to "food safety". Clearly, the interactions of diet/food with the genetic background, gender, and developmental state of the individual, together with (a) interactions of other endogenous/exogenous chemicals/drugs; (b) the specific biology of the cells being affected; (c) the mechanisms by which the presence or absence of toxins/toxicants and nutrients work to cause toxicities; and (d) how those mechanisms affect the pathogenesis of acute and/or chronic diseases, must be integrated into a "system" approach. Mechanisms of how toxins/toxicants cause cellular toxicities, such as mutagenesis; cytotoxicity and altered gene expression, must take into account (a) irreversible or reversal changes caused by these toxins or toxicants; (b)concepts of thresholds or no-thresholds of action; and (c) concepts of differential effects on stem cells, progenitor cells and terminally differentiated cells in different organs. This brief Commentary tries to illustrate this complex interaction between what is on/in foods with one disease, namely cancer. Since the understanding of cancer, while still incomplete, can shed light on the multiple ways that toxins/toxicants, as well as dietary modulation of nutrients/vitamins/metals/ calories, can either enhance or reduce the risk to cancer. In particular, diets that alter the embryo-fetal micro-environment might dramatically alter disease formation later in life. In effect "food safety" can not be assessed without understanding how food could be 'toxic', or how that mechanism of toxicity interacts with the pathogenesis of any disease.