• Asian-Australasian Journal of Animal Sciences
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• 제15권7호
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• pp.1051-1056
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• 2002

In vitro binding efficacy of esterified glucomannan (E-GM) (0.1%) on aflatoxin B1 (AF) (300 ppb), ochratoxin A (OA) (2 ppm) and T-2 toxin (T-2) (3 ppm), when present alone or in combination, was evaluated in toxin-contaminated feed at pH 4.5 and 6.5. Esterified glucomannan showed significantly (p<0.01) higher binding with AF (81.6%), whereas those recorded with T-2 (27.8%) and OA (25.6%) were moderate. Binding of each toxin decreased as the number of toxins in feed increased. pH of medium showed no effect on mycotoxin binding ability of E-GM. A $2{\times}2{\times}2{\times}2$ factorial experiment of 5 week duration was conducted to study the effects of two dietary levels each of AF (0 and 300 ppb), OA (0 and 2 ppm), T-2 (0 and 3 ppm ) and E-GM (0 and 0.1%) on the immune competence of a total of 960 day-old commercial broilers. Reductions in size of thymus (by AF and T-2) and bursa (by AF) and antibody titers against Newcastle disease and Infectious Bursal disease (by all the toxins) were noted. Additive and antagonistic interactions were seen among the toxins on certain parameters. Esterified glucomannan significantly (p<0.01) improved antibody titers and weights of bursa ofFabricius and thymus indicating its counteracting efficacy against immunosuppression in mycotoxicosis of multiple origin.

• Journal of Digestive Cancer Research
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• 제1권2호
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• pp.82-88
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• 2013

Cancer is the first leading cause of death in Korea and the second leading cause of death in the USA. There is extensive research into prevention of cancer and the support of oncology patients with diet or dietary supplements. In vitro and in vivo animal studies have indicated that antioxidants, including beta-carotene, alpha-tocopherol, and ascorbic acid, can yield anti-cancer effects in addition to providing protection against oxidative damage. Although many observational studies have shown that consuming fruits and vegetables can reduce the risk of some cancers, the results of several large-scale human intervention trials testing the benefits of a single or combined higher-dose of individual micronutrients have been inconsistent. Cancer can cause profound metabolic and physiological changes which may affect patients' nutrient requirements. Although the optimal route of nutrient delivery is through diet, cancer patients often suffer symptoms that disrupt their food intake, including anorexia, premature satiety, altered taste and smell, and changes in bowel mobility. In particular, micronutrient deficits can slow postoperative healing, contribute to depression symptoms, and decrease immune competence. Cancer patients are generally motivated to take dietary supplements to improve responses to treatment and quality of life. The Physician's Health Study II (PHS II) randomized controlled trial reported recently that daily multivitamin supplementation significantly, albeit modestly, reduced the risk of total cancer. Although evidence of multivitamin use benefits is limited in cancer patients, taking dietary supplements with constituents in the range of the recommended daily allowance according to the Dietary Reference Intake (DRI) recommendation is generally considered to be safe.

• 대한미생물학회지
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• 제21권3호
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• pp.311-329
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• 1986

The experimental exposure of animals to sources of ultraviolet radiation (UVR) which emit their energy primarily in the UVB region (280-320nm) is known to result in a number of well-described changes in the recipient's immune competence. Two such changes include a depressed capacity to effectively respond immunologically to transplants of syngeneic UVR tumors and a markedly reduced responsiveness to known inducers of delayedtype (DTH) and contact hypersensitivity (CH) reactions. The results of experiments that were designed to elucidate the mechanisms responsible for UVR-induced immunomodulation have implicated: 1) an altered pattern of lymphocyte recirculation, 2) suppressor T cells(Ts), 3) deviations in systemic antigen presenting cell (APC) potential. 4) changes in the production of interleukin-1-like molecules, and 5) the functional inactivation of epidermal Langerhans cells in this process. The exposure of skin to UVR, therefore, causes a number of both local and systemic alterations to the normal host immune system. In spite of this seeming complexity and diversity of responses, our recent studies have established that each of the UVR-mediated changes is probably of equal importance to creating the UVR-induced immunocompromised state. Normal animals were exposed to low dose UVR radiation on their dorsal surfaces under conditions where a $3.0\;cm^2$ area of skin was physically protected from the light energy. Contact sensitization of these animals with DNFB, to either the irradiated or protected back skin, resulted in markedly reduced CH responses. This was observed in spite of a normal responsiveness following the skin sensitization to ventral surfaces of the UVR-exposed animals. Systemic treatment of the low dose UVR recipients with the drug indomethacin (1-3 micrograms/day) during the UVR exposures resulted in a complete reversal of the depressions observed following DNFB sensitization to "protected" dorsal skin while the altered responsiveness found in the group exposed to the skin reactive chemical through directly UVR-exposed sites was maintained. These studies implicate the importance of EC as effective APC in the skin and also suggest that some of the systemic influences caused by UVR exposure involve the production of prostaglandins. This concept was further supported by finding that indomethacin treatment was also capable of totally reversing the systemic depressions in CH responsiveness caused by high dose UVR exposure (30K joules/$m^2$) of mice. Attempts to analyze the cellular mechanisms responsible established that the spleens of all animals which demonstrated altered CH responses, regardless of whether sensitization was through a normal or an irradiated skin site, contained suppressor cells. Interestingly, we also found normal levels of T effector cells in the peripheral lymph nodes of the UVR-exposed mice that were contact sensitized through normal skin. No effector cells were found when skin sensitization took place through irradiated skin sites. In spite of such an apparent paradox, insight into the probable mechanisms responsible for these observations was provided by establishing that UVR exposure of skin results in a striking and dose-dependent blockade of the efferent lymphatic vessels in all peripheral lymph nodes. Therefore, the afferent phases of immune responses can apparently take place normally in UVR exposed animals when antigen is applied to normal skin. The final effector responses, however, appear to be inhibited in the UVR-exposed animals by an apparent block of effector cell mobility. This contrasts with findings in the normal animals. Following contact sensitization, normal animals were also found to simultaneously contain both antigen specific suppressor T cells and lymph node effector cells. However, these normal animals were fully capable of mobilizing their effector cells into the systemic circulation, thereby allowing a localization of these cells to peripheral sites of antigen challenge. Our results suggest that UVR is probably not a significant inducer of suppressor T-cell activity to topically applied antigens. Rather, UVR exposure appears to modify the normal relationship which exists between effector and regulatory immune responses in vivo. It does so by either causing a direct reduction in the skin's APC function, a situation which results in an absence of effector cell generation to antigens applied to UVR-exposed skin sites, inhibiting the capacity of effector cells to gain access to skin sites of antigen challenge or by sequestering the lymphocytes with effector cell potential into the draining peripheral lymph nodes. Each of these situations result in a similar effect on the UVR-exposed host, that being a reduced capacity to elicit a CH response. We hypothesize that altered DTH responses, altered alloresponses, and altered graft-versus-host responses, all of which have been observed in UVR exposed animals, may result from similar mechanisms.

• 한국식물병리학회:학술대회논문집
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• 한국식물병리학회 2003년도 정기총회 및 추계학술발표회
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• pp.148.2-149
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• 2003

Cucumber fruit mottle mosaic tobamovirus (CFMMV) causes severe mosaic symptoms with yellow mottling on leaves and fruits, and occasionally severe wilting of cucumber plants. No genetic source of resistance against this virus has been identified. The genes coding for the coat protein or the putative 54-kDa replicase were cloned into binary vectors under control of the SVBV promoter. Agrobacterium-mediated transformation was peformed on cotyledon explants of a parthenocarpic cucumber cultivar with superior competence for transformation. R1 seedlings were evaluated for resistance to CFMMV infection by lack of symptom expression, back inoculation on an alternative host and ELISA. From a total of 14 replicase-containing R1 lines, 8 exhibited immunity, while only 3 resistant lines were found among a total of 9 CP-containing lines. Line 144 homozygous for the 54-kDa replicase was selected for further resistance analysis. Line 144 was immune to CFMMV infection by mechanical and graft inoculation, or by root infection following planting in CFMMV-contaminated soil. Additionally, line 144 showed delay of symptom appearance following infection by other cucurbit-infecting tobamoviruses. Infection of line 144 plants with various potyviruses and cucumber mosaic cucumovirus did not break the resistance to CFMMV. The mechanism of resistance of line 144 appears to be RNA-mediated, however the means is apparently different from the gene silencing phenomenon. Homozygote line 144 cucumber as rootstock demonstrated for the first time protection of a non-transformed scion from soil inoculation with a soil borne pathogen, CFMMV.

• Asian-Australasian Journal of Animal Sciences
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• 제18권1호
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• pp.80-84
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• 2005

An experiment was conducted to study the performance, carcass traits, serum lipid profile and immune competence in commercial broilers (2 to 42 d of age) fed graded levels (25, 50, 75 and 100%) of finger millet (FM) (Elusine coracana) in place (w/w) of yellow maize (YM). Each diet was fed to eight replicates (five female Vencobb broilers/replicate) housed in stainless steel battery brooders. The estimated metabolizable energy content of FM was about 540 kcal less than the YM. FM contained more protein (10.42 vs. 9.05%) and fibre (9.52 vs. 2.24%) compared to YM. Body weight gain, ready to cook yield, relative weights of giblet, liver, intestine and length of intestine at 42 d of age was not affected due to replacing YM with FM. But, the feed efficiency decreased in broilers fed diets containing 75 and 100% FM in place of YM at both 21 and 42 d of age. The amount of fat deposited in abdominal area decreased and the relative weight of gizzard increased with increase in level of FM in the diet. The serum HDL cholesterol at 21 and 42 d of age and serum triglycerides at 42 d of age decreased with increase in level of FM in diet. The relative weight of spleen and antibody titers against sheep red blood cells (SRBC) at 5 d post inoculation (PI) decreased in broilers fed FM at 100% of YM. However, the relative weight of bursa, SRBC titers at 10 d PI, antibody titers against ND virus and mortality were not affected due to incorporation of FM in place of YM in diet. The fat content in thigh muscle and liver decreased, while the protein content in these tissues increased with increase in the level of FM in broiler diet. Based on the results, it may be concluded that YM can be replaced with FM up to 25% on weight basis without affecting weight gain, carcass yields and immunity in commercial broiler diet (up to 42 d of age). Further, inclusion of finger millet reduced the fat deposition in thigh muscle, liver and in abdominal area compared to those fed maize as the principal source of energy.

• 대한수의학회지
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• 제35권2호
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• pp.405-416
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• 1995

말의 뇌화연증(equine leukoencephalomalacia)과 돼지의 폐수종(porcine pulmonary edema)은 Fusarium에 오염된 옥수수로 인하여 발생되는 것으로 추정되어 왔다. 1988년에 F moniliforme에서 2차 대사산물인 fumonisin $B_1(FB_1)$이 동정되면서 오염된 옥수수와 순수 분리된 $FB_1$으로 두질병이 실험적으로 재현되었고, 말과 돼지 이외의 다른 가축에 대해서도 독성 연구가 진행되고 있다. fumonisins(FBs)는 모든 종에서 간에 독성을 나타내나 종에 따라 주요 독성 장기가 각기 다름이 밝혀지고 있다. FB의 독성 기전에 대해서는 잘 알려지지 않았으나 FB가 sphingolipid 생성과정을 차단함으로써 장기 및 혈중에 sphinganine(SA) : sphingosine(SO)를 증가시키는 것으로 알려졌다. 이는 증가된 SA : SO가 FB 독성의 진단기준이 될 수 있음을 시사하는 것이다. 최근 진행 중인 연구에 의하면, 저용량의 $FB_1$ 급식 투여가 돼지에서 혈중 입자(blood-born particle)에 대한 폐혈관 대식 세포(pulmonary intravascular macrophage)의 탐식 능력을 저하시켜, 세균 감염에 대한 감수성이 증가될 수 있음을 시사하고 있다. Fusarium 속균은 전세계적으로 생산되는 옥수수에서 발생되고 있으며, 우리나라는 사료에 사용되는 옥수수의 절대량을 수입에 의존하고 있는 점을 고려할 때, 허용기준 및 무해용량 등에 대한 관리가 절실하다. 이 논문에서는 최근 연구된 FB에 의한 가축 독성에 대하여 기술하고자 한다.

• 대한미생물학회지
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• 제35권2호
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• pp.191-201
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• 2000

The viruses of Herpes Simplex Virus 1 (HSV-1), Herpes Simplex Virus 2 (HSV-2) and Varicella-Zoster virus (VZV) which belong to the alpha herpes subfamily are important human pathogens. When eruptions were not fully developed from these viral infections, clinical diagnosis was not always easy and required virological confirmation test. The above viruses were reactivated in individuals who were compromised in immune competence for one reason or another. Polymerase chain reaction (PCR) enables rapid and sensitive detection of HSV and VZV DNAs. Its sensitivity was largely influenced by choice of primers. Authors conducted a study to detect of those three viruses in human specimens including vesicle fluid and joint fluid and serum using PCR methods. Primers used for this study were the general primer pair GPHV-RU which was known to amplify within the genes enjoying the highest degree of homology between UL15 of HSV and UL42 of VZV. PCR with primers hybridized pair GPHV-RU amplifies a 396 bp with THP-1 and HSV-2 standard strain DNA and 405 bp with VZV standard strain DNA. Restriction enzyme cleavage with HpaII and DdeI were used to detect and distinguish DNAs of THP-1 and HSV-2 and VZV. The purpose of this study was a rapid and easy detection of VZV and THP-1 or HSV-2 from various clinical specimens (vesicle fluid, serum and joint fluid) by PCR method. Used methods were: HSV PCR with primer 1, 2 and HpaII RE digestion; VZV nested PCR; HSV PCR with primer A, Band BssHII RE digestion. 1) In 33 cases (33/42, 78.6%) VZV was detected single or mixed infection from 42 clinical specimens which included vesicle fluid (5), serum form respiratory infected children (10), serum from immune suppressed adult cancer patients (7) and joint fluid from arthritis patients (20). 2) In 20 cases (20/42, 47.6%) HSV was detected singly or mixed infection and 19 of those cases were HSV-2 and 1 case was THP-1. 3) In 19 cases (19/42, 45.2%) VZV was singly detected which included serum from respiratory infected children (6 cases), joint fluid from arthritis patients (9 cases), vesicle fluid (2 cases) and serum form immunosuppressed cancer patients (2 cases). 4) HSV was singly detected in 6 cases (6/42, 14.3%) which included joint fluid from arthritis patients (5 cases) and serum form respiratory infected children (1 cases). 5) 14 cases of VZV and HSV mixed infection (14/42, 33.3%) were detected. They included vesicle fluid (3 cases), serum form immunosuppressed cancer patients (4 cases), serum from respiratory infected children (2 cases) and joint fluid from arthritis patients (5 cases). 6) HSV-1 and HSV-2 detection and typing by HSV PCR with primer A, Band BssHII RE digestion method was more sensitive and the results were easier to detect than on other method.