• Journal of Animal Science and Technology
• /
• v.50 no.2
• /
• pp.265-272
• /
• 2008

The CCAAT/enhancer binding protein β(C/EBPβ), a member of the leucine zipper DNA-binding protein of transcription factor, plays a crucial role in the control of early phases of adipocyte differentiation. In this studies, we report the identification, characterization, and expression of the Korean native cattle C/EBPβ gene. The Korean native cattle and black cattle C/EBPβ cDNA includes a 1047bp open reading frame encoding a protein of 348 amino acids. The C/EBPβ cDNA sequence of the Korean native cattle and black cattle shows high conservation with the corresponding amino acid sequences reported in other species. The distribution of C/EBPβ mRNA in various tissues of Korean native cattle aged 26 months was investigated using Northern Blot analysis. The C/EBPβ expression was detected in adipose tissue, lung, sirloin while expression was not detected in heart, kidney, small intestine, colon, and liver. However, we are analyzed polymorphism of bZIP domain in the C/EBPβ gene. A polymorphism was not identified at this position.

• Korean Journal of Fisheries and Aquatic Sciences
• /
• v.14 no.4
• /
• pp.217-220
• /
• 1981

A trematode, Cercaria tapidis which is parasitic to short necked clam, Tapes philippinarum was studied in terms of its morphology and incidence of infection rate. The host bivalve was collected from Solri near Gunsan from September 1980 to August 1981. Sporocysts were observed mainly in tissues of gonad of the short necked clams. Minimum infection rate ($0.85\%$) was found in May, while maximum infection rate ($23.27\%$) in December. The sporocyst is 1.1 mm long and 0.27 mm wide. Ellipsoidal body of cercaria is $283{\mu}m$ long and $120{\mu}m$ wide. Oral sucker is much larger than ventral sucker. Moderately small pharynx, a long esophagus, and a long intestine reaching to the posterior end of the body are distinctive. Globular excretory bladder is located at the posterior part of the body and bears numerous granules of various size. The flame-cell arrangement is represented by a formula 2[(3+3+3)+(3+3)]=30. Tail is five times body length.

• YAKHAK HOEJI
• /
• v.42 no.4
• /
• pp.437-446
• /
• 1998

The distribution, metabolism and excretion of CKD-602{20(S)-7-[2-(N-Isopropylamino)ethyl]camptothecin HCI), a new camptothecin derivative, were investigated in rats after a sing le administration of CKD-602. 1. The tissue levels of CKD-602 given to mice by the intravenous route at a dose of 20mg/kg were the highest in intestine, followed in descending order by kidney, liver, stomach,lung, heart, spleen and plasma. The concentrations of CKD-602 after 24hrs decreased to less than 2% of the peak level in most tissues except the skin. The urinary and fecal excretion of CKD-602 were 47.6% and 44.4% of the administered dose, respectively, with 0.7% remaining in the rinse. 2. After administration of CKD-602 at 10mg/kg in rats, metabolism of this compound was examined in plasma, urine, and feces. The plasma samples were collected for 24hr, urinary and fecal samples for 72hr. While any peak of CKD-602 in HPLC chromatograms was not detected from plasma and urine it was detected in feces (peaks, 9.8 min). However, additional peak area was about 0.5% of the peak area of parent CKD-602. Therefore, CKD-602 may be eliminated with the parent form and rarely metabolized in the body. 4. After I.v. administration of CKD-602 at 10mg/kg in rats, urinary and fecal excretions were examined for 72hrs post dose period. 87% of total urinary excretion of CKD-602 was excreted within 8hr after administration, 53%, and 32% of total fecal excreted amounts were determined in 0-24 hr and 24-48hr periods, respectively. The total excretion amounts of CKD-602 into urine and feces were 94% of the administered dose.

• Journal of Microbiology and Biotechnology
• /
• v.26 no.8
• /
• pp.1446-1451
• /
• 2016

Clostridium difficile toxin A causes acute gut inflammation in animals and humans. It is known to downregulate the tight junctions between colonic epithelial cells, allowing luminal contents to access body tissues and trigger acute immune responses. However, it is not yet known whether this loss of the barrier function is a critical factor in the progression of toxin A-induced pseudomembranous colitis. We previously showed that NADH:quinone oxidoreductase 1 (NQO1) KO (knockout) mice spontaneously display weak gut inflammation and a marked loss of colonic epithelial tight junctions. Moreover, NQO1 KO mice exhibited highly increased inflammatory responses compared with NQO1 WT (wild-type) control mice when subjected to DSS-induced experimental colitis. Here, we tested whether toxin A could also trigger more severe inflammatory responses in NQO1 KO mice compared with NQO1 WT mice. Indeed, our results show that C. difficile toxin A-mediated enteritis is significantly enhanced in NQO1 KO mice compared with NQO1 WT mice. The levels of fluid secretion, villus disruption, and epithelial cell apoptosis were also higher in toxin A-treated NQO1 KO mice compared with WT mice. The previous and present results collectively show that NQO1 is involved in the formation of tight junctions in the small intestine, and that defects in NQO1 enhance C. difficile toxin A-induced acute inflammatory responses, presumably via the loss of epithelial cell tight junctions.

• Korean Journal of Poultry Science
• /
• v.50 no.2
• /
• pp.109-118
• /
• 2023

Four-d-old broiler chicks were randomly assigned to 3 groups with 9 replicates (8 birds/cage) under high ambient temperature; birds fed a basal diet (CON), a basal diet supplemented with 0.25% of probiotic complex (LPB, 1 × 10⁶ Lactobacillus plantarum, 1 × 10⁶ Bacillus subtilis, and 1 × 10⁶ Saccharomyces cerevisiae) and 0.5% probiotic complex (HPB). Immediately after 28-d feeding trial, 6 birds having average body weight per group were sacrificed for evaluating the effects of probiotics on antioxidant parameters in the serum, intestine, and liver of birds. As results, serum biochemical parameters of nitrogen components including total protein, albumin, urea nitrogen, and glutathione were unaffected by dietary probiotics. In addition, serum superoxide dismutase (SOD), glutathione peroxidase (GPX), and glutathione S-transferase (GST) activities, and lipid peroxidation (MDA) were not changed by dietary probiotic supplement in birds. In the intestinal mucosa, SOD activity in the HPB group significantly (P<0.05) increased compared with that in the CON and the LPB groups. Lipid peroxidation in the HPB group significantly (P<0.05) decreased compared with that in the CON group. However, there was no statistical difference in GPX, and GST activities in the intestinal mucosa among treatment groups. In the liver, the activities of SOD, GPX, and GST, and the level of MDA were unaffected by probiotic supplement. In conclusion, 0.5% of probiotics significantly increased SOD activity and decreased lipid peroxidation in the intestinal mucosa, suggesting that probiotic complex could be potential to improve the small intestinal antioxidant capacity of bird under high ambient temperature conditions.

• Animal Bioscience
• /
• v.35 no.10
• /
• pp.1461-1478
• /
• 2022

The maintenance of poultry gut health is complex depending on the intricate balance among diet, the commensal microbiota, and the mucosa, including the gut epithelium and the superimposing mucus layer. Changes in microflora composition and abundance can confer beneficial or detrimental effects on fowl. Antibiotics have devastating impacts on altering the landscape of gut microbiota, which further leads to antibiotic resistance or spread the pathogenic populations. By eliciting the landscape of gut microbiota, strategies should be made to break down the regulatory signals of pathogenic bacteria. The optional strategy of conferring dietary fibers (DFs) can be used to counterbalance the gut microbiota. DFs are the non-starch carbohydrates indigestible by host endogenous enzymes but can be fermented by symbiotic microbiota to produce short-chain fatty acids (SCFAs). This is one of the primary modes through which the gut microbiota interacts and communicate with the host. The majority of SCFAs are produced in the large intestine (particularly in the caecum), where they are taken up by the enterocytes or transported through portal vein circulation into the bloodstream. Recent shreds of evidence have elucidated that SCFAs affect the gut and modulate the tissues and organs either by activating G-protein-coupled receptors or affecting epigenetic modifications in the genome through inducing histone acetylase activities and inhibiting histone deacetylases. Thus, in this way, SCFAs vastly influence poultry health by promoting energy regulation, mucosal integrity, immune homeostasis, and immune maturation. In this review article, we will focus on DFs, which directly interact with gut microbes and lead to the production of SCFAs. Further, we will discuss the current molecular mechanisms of how SCFAs are generated, transported, and modulated the pro-and anti-inflammatory immune responses against pathogens and host physiology and gut health.

• Korean Journal of Poultry Science
• /
• v.29 no.4
• /
• pp.237-241
• /
• 2002

To observe the effect of Induced molting on the recovery patterns of abdominal fat, visceral organs, and muscle tissues in spent laying hens after induced molting, three hundred sixty 77-wk-old, Babcock White hens were divided into 36 experimental units of 10 hens each and subjected to molt induction for seven wk. The post-molt production phase was spread over 84 to 126 wks of age. Thirty-six birds were randomly slaughtered and dressed at the pre-molt, 5% egg production, Peak, and end Phases of e99 Production. The body weight, abdominal fat, relative weight and length of visceral organs were measured. Proximate compositions of breast and thigh muscles were analyzed at each stage. The body weight was found to be minimal at the 5% egg Production stage, but increased as the egg Production increased for the rest of production. The pattern of abdominal fat change was very similar to that of body weight. The relative weight of the liver decreased to the lowest at the start of Post molting stage, but Peaked at the end Phase of egg Production (P<0.05). However, he heart and gizzard were observed to reach their maximum weight at the 5% egg Production (P<0.05), whereas they were, similar to those of the pre-molt phase for the rest of the production stages. Both intestine and reproductive tracts were found o be significantly smaller at 5% egg Production than at the other stages; however, their sizes increased gradually, reaching leak at the end Phase of e99 Production (P<0.05). Fat contents in breast and thigh muscles decreased significantly to the lowest at the start of the Post-molt stage, but increased to the highest at the end Phase of e99 Production (P<0.05). Thus, he Present study indicated that the molting process reduced body weight by decreasing the weights of abdominal fat and other visceral organs. Molting also influenced the breast and thigh muscle composition by decreasing fat content.

• Archives of Pharmacal Research
• /
• v.28 no.3
• /
• pp.249-268
• /
• 2005

Drug metabolizing enzymes (DMEs) play central roles in the metabolism, elimination and detoxification of xenobiotics and drugs introduced into the human body. Most of the tissues and organs in our body are well equipped with diverse and various DMEs including phase I, phase II metabolizing enzymes and phase III transporters, which are present in abundance either at the basal unstimulated level, and/or are inducible at elevated level after exposure to xenobiotics. Recently, many important advances have been made in the mechanisms that regulate the expression of these drug metabolism genes. Various nuclear receptors including the aryl hydrocarbon receptor (AhR), orphan nuclear receptors, and nuclear factor-erythoroid 2 p45-related factor 2 (Nrf2) have been shown to be the key mediators of drug-induced changes in phase I, phase II metabolizing enzymes as well as phase III transporters involved in efflux mechanisms. For instance, the expression of CYP1 genes can be induced by AhR, which dimerizes with the AhR nuclear translocator (Arnt) , in response to many polycyclic aromatic hydrocarbon (PAHs). Similarly, the steroid family of orphan nuclear receptors, the constitutive androstane receptor (CAR) and pregnane X receptor (PXR), both heterodimerize with the ret-inoid X receptor (RXR), are shown to transcriptionally activate the promoters of CYP2B and CYP3A gene expression by xenobiotics such as phenobarbital-like compounds (CAR) and dexamethasone and rifampin-type of agents (PXR). The peroxisome proliferator activated receptor (PPAR), which is one of the first characterized members of the nuclear hormone receptor, also dimerizes with RXR and has been shown to be activated by lipid lowering agent fib rate-type of compounds leading to transcriptional activation of the promoters on CYP4A gene. CYP7A was recognized as the first target gene of the liver X receptor (LXR), in which the elimination of cholesterol depends on CYP7A. Farnesoid X receptor (FXR) was identified as a bile acid receptor, and its activation results in the inhibition of hepatic acid biosynthesis and increased transport of bile acids from intestinal lumen to the liver, and CYP7A is one of its target genes. The transcriptional activation by these receptors upon binding to the promoters located at the 5-flanking region of these GYP genes generally leads to the induction of their mRNA gene expression. The physiological and the pharmacological implications of common partner of RXR for CAR, PXR, PPAR, LXR and FXR receptors largely remain unknown and are under intense investigations. For the phase II DMEs, phase II gene inducers such as the phenolic compounds butylated hydroxyanisol (BHA), tert-butylhydroquinone (tBHQ), green tea polyphenol (GTP), (-)-epigallocatechin-3-gallate (EGCG) and the isothiocyanates (PEITC, sul­foraphane) generally appear to be electrophiles. They generally possess electrophilic-medi­ated stress response, resulting in the activation of bZIP transcription factors Nrf2 which dimerizes with Mafs and binds to the antioxidant/electrophile response element (ARE/EpRE) promoter, which is located in many phase II DMEs as well as many cellular defensive enzymes such as heme oxygenase-1 (HO-1), with the subsequent induction of the expression of these genes. Phase III transporters, for example, P-glycoprotein (P-gp), multidrug resistance-associated proteins (MRPs), and organic anion transporting polypeptide 2 (OATP2) are expressed in many tissues such as the liver, intestine, kidney, and brain, and play crucial roles in drug absorption, distribution, and excretion. The orphan nuclear receptors PXR and GAR have been shown to be involved in the regulation of these transporters. Along with phase I and phase II enzyme induction, pretreatment with several kinds of inducers has been shown to alter the expression of phase III transporters, and alter the excretion of xenobiotics, which implies that phase III transporters may also be similarly regulated in a coordinated fashion, and provides an important mean to protect the body from xenobiotics insults. It appears that in general, exposure to phase I, phase II and phase III gene inducers may trigger cellular 'stress' response leading to the increase in their gene expression, which ultimately enhance the elimination and clearance of these xenobiotics and/or other 'cellular stresses' including harmful reactive intermediates such as reactive oxygen species (ROS), so that the body will remove the 'stress' expeditiously. Consequently, this homeostatic response of the body plays a central role in the protection of the body against 'environmental' insults such as those elicited by exposure to xenobiotics.

• Radiation Oncology Journal
• /
• v.22 no.4
• /
• pp.288-297
• /
• 2004

Puporse: The aims of this study were to evaluate the change of $[^18F]fluoromisonidazole$($[^18F]FMISO$) uptake in C3H mouse squamous cell carcinoma-VII (SCC-VII) treated with mild hyperthermia ($42^{circ}C$) and nicotinamide and to assess the biodistribution of the markers in normal tissues under similar conditions. Methods and Materials: $[^18F]FMISO$ was producedby our hospital. Female C3H mice with a C3H SCC-VII tumor grown on their extremities were used. Tumors were size matched. Non-anaesthetized, tumor-bearing mice underwent control or mild hyperthermia at $42^{circ}C$ for 60 min with nicotinamide (50 mg/kg i.p. injected) and were examined by gamma counter, autoradiography and animal PET scan 3 hours after tracer i.v. injected with breathing room air, The biodistribution of these agents were obtained at 3 h after $[^18F]FMISO$ injection. Blood, tumor, muscle, heart, lung, liver, kidney, brain, bone, spleen, and intestine were removed, counted for radioactivity and weighed. The tumor and liver were frozen and cut with a cryomicrotome into 10- um sections. The spatial distribution of radioactivity from the tissue sections was determined with digital autoradiography. Results: The mild hyperthermia with nicotinamide treatment had only slight effects on the biodistribution of either marker in normal tissues. We observed that the whole tumor radioactivity uptake ratios were higher in the control mice than in the mild hyperthermia with nicotinamide treated mice for $[^18F]FMISO$ ($1.56{\pm}1.03$ vs. $0.67{\pm}0.30$; p=0.063). In addition, autoradiography and animal PET scan demonstrated that the area and intensity of $[^18F]FMISO$ uptake was significantly decreased. Conclusion: Mild hyperthermla and nicotinamide significantly improved tumor hypoxia using $[^18F]FMISO$ and this uptake reflected tumor hypoxic status.

• Parasites, Hosts and Diseases
• /
• v.27 no.2
• /
• pp.109-118
• /
• 1989

Production of circulating specific antibodies to the lung fluke (Paragenimus westermani) by its host is well known and used in various kinds of immunodiagnostic methods, However, it has not been well documented which compartments (or structures) of the lung fluke are most responsible for the production of specific antibodies. The present immunohistochemical study was undertaken to demonstrate the antigenicity of each body compartment of p. westermani such as suckers, tegument, spines, vitelline glands, intestine, reproductive organs(male and female), and eggs. Indiret immunoperoxidase(IP) stain technique was applied, using formalin-fked, paraffin- embedded lung tissues of P westermani-infected cats sectioned in 4 Um thickness as the antigen and cat antisera (11~20 weeks of infection) as the primary antibody. Peroxidase-conjugated goat anti-cat IgG was used as the secondary antibody and diaminobensidine(DAB) as the coloring agent. Strong yellow or yellowish brown staining was regarded positive. The primary and secondary antibody dilutions were made at 1 : 500~1 : 2, 000 and 1 : 200~1 : 500 respectively, and IP stain was repeated 10 times for each dilution. A consistent result obtained was that the intestinal epithelial border, intestinal content, vitelline glands, and eggs scattered around the worm capsule showed strong positive staining, while uterine eggs and some parenchymal portions showed weak positive reaction. On the other hand, the suckers, tegument, spines, subtegumental cells, cytoplasm of intestinal epithelial cells, male reproductive organs, and ovary revealed negative staining. The body compartments showing higher antigenicity were, in the decreasing order, the intestinal epithelial border, intestinal content, eggs in the worm capsule, vitelline glands, uterine eggs, and parenchymatous portions. The intestinal epithelial border and luminal contents revealed positive staining even at a few concentration of 1 : 4, 000 primary antibody(secondary ab., 1 : 200) whereas the parenchymatous portion showed positive reaction only at higher concentrations than 1'500 (secondary ab., 1 : 200). The results suggest that the specific antibody responses of the host to p. westermani occur most strongly upon the excretes from the intestinal epithelium of the worm and e99s Produced around the worm capsule,