A disease of young Holstein calves characterized by recurrent pneumonia, ulcerative and granulomatous stomatitis, enteritis with bacterial overgrowth, periodontitis, delayed wound healing, persistent neutrophilia and death at an early age had been originally described in 1983 and again in 1987. Most of these calves had stunted growth and a persistent, progressive neutrophilia (often exceeding 100,000/ml). By investigation of pedigrees, all of the affected calves have now been traced to a common sire and confirmed by polymerase chain reaction (PCR) diagnostic DNA testing to be homozygous carriers of a defective allele for bovine CD18. Neutrophils from these calves have several functional deficits and, most importantly, fail to adhere in a ${\beta}_2$-integrin dependent manner. The ${\beta}_2$-integrins represent a family of glycoproteins which participate in various leukocyte adhesion reactions during host defense. The presence or absence of ${\beta}_2$-integrin molecules can be demonstrated on the surface of neutrophils, monocytes and lymphocytes from normal or affected calves using specific monoclonal antibodies and flow cytometry, or by colloidal gold immunolabeling and scanning electron microscopy in backscatter mode. Deficiency of the ${\beta}_2$-integrins on all leukocyte types in Holstein calves is analogous to leukocyte adhesion deficiency (LAD) seen in humans. Neutrophils in bovine (BLAD) and human LAD patients are unable to adhere to the endothelial lining of the cardiovascular system thus interrupting egression of neutrophils into infected tissues. Other leukocytes, while still deficient in expression of the ${\beta}_2$-integrins, are still able to efficiently egress from the blood stream due to interactions of other adhesion molecules that are not as highly expressed on neutrophils. Both BLAD cattle and LAD children (who do not receive bone marrow transplants) often die at an early age as a result of the failure of neutrophils to extravasate into infected tissues. In 1991, Shuster, et $al^{27}$, identified two point mutations within the alleles encoding bovine CD18 in a Holstein calf afflicted with leukocyte adhesion deficiency. One mutation causes an aspartic acid to glycine substitution at amino acid 128 (D128G) in an extracellular region of this adhesion glycoprotein that is highly conserved (> 95% identity) between humans, cattle and mice. The other mutation is silent. Numerous calves with clinical symptoms of leukocyte adhesion deficiency have since been tested and all have been found homozygous for the D128G allele. In addition, calves homozygous far the D128G allele have been identified during widespread DNA testing in the United States. All cattle with the mutant allele are related to one bull, who through artificial insemination (A.I.), sired many calves in the 1950's and 1960's. The carrier frequency of the D128G CD18 allele among U.S. Holstein cattle had reached approximately 15% among active A.I. bulls and 8% among cows. By 1993, the organization of the dairy industry and the diagnostic test developed to genotype cattle, enabled virtually complete eradication of bovine leukocyte adhesion deficiency among current and future A.I. bulls.
The purpose of the present study was to understand the pathogenesis of infections in piglets inoculated with C parvum isolated from mice alone and combined with porcine rotavirus (S-80). Thirteen 10-day piglets were divided in four groups; Three, A group, were only given by C parvum. Four, B group, were orally administrated with firstly porcine rotavirus and then C patvum. Three, C group, were orally inoculated with porcine rotavirus alone. The rest, D group, were used as controls. During the experiment, there were daily recorded clinical signs including diarrhea to each pig. According to the periodic intervals for necropsy, all pigs were sacrificed from 4 to 12 days after the final inoculation of C parvum. Location and distribution of two pathogens, C parvum and rotavirus, in the intestinal mucosa of piglets tested were examined by pathological and immunohistological means. In addition, parasitological test using the feces of piglets was applied for the detection of cryptosporidial oocysts as well. A group showed diarrhea from 4 to 6 days post-inoculation(PI) and also discharged C parvum oocysts in feces during the day 4 to 7 PI. In tissue sections of jejunum and ileum, cryptosporidial oocysts were observed a few on the top of villi with slightly fusion. B group represented sign of diarrhea and discharge of oocysts from 2 to 11 days PI. There were some cryptosporidial oocysts both in the jejunal lumen and in the lumen of mucosal glands. As progressed, oocysts were most commonly distributed on the tip of villi of jejunum. Histopathologically there were also mild to moderately fused, attenuated focal desquamated, congested villi and mononuclear cell infiltration of varying degrees in the lamina propria of small intestine and colon at the day 4 and 7 PI. C group showed slightly to mildly attenuated and fused top of villi and mildly mucosal congestion. D group as controls was grossly and histopathologically normal in all parts of intestine. The present results indicate that the piglets inoculated with C parvum only are certainly milder in pathogenesis including duration of clinical course and severity of lesion than those in piglets concurrently infected with porcine rotavirus and C parvum. Also the strain (VRI-CN91) of C parvum used in the study has very low pathogenicity to occur enteritis of piglets.
The objective of this study was to investigate the in vitro / in vivo embryonic development after vitrification of mouse zygotes and the chrom osomal normality of delivered live young after embryo transfer. Mouse IVF zygotes were cryopreserved by vitrification using vitrification solution, EFS40 (40% ethylene glyc이, 30% Ficoll a and 0.3 M sucrose in phosphate buffer saline c containing 10% FBS ) . After mouse zygotes were exposed to EFS40 at 25"C for 30 sec., they were immediately plunged into LN$_2$. Vitrified thawed mouse zygotes were cultured upto bIastocysts in M16 for 4 days. The rates of in vitro development were 71.5% under this condition. Cultured blastocysts were transferred to recipients (3 day of pseudopregnant) on one or both uterus horns (6-8 embryos per a uterus horn). And all recipients were allowed to produce litters. The results obtained in these experiments were summarized as follows: The pregnancy rates and in vivo survival rates, live fetus rates, for vitrified zygotes (80.0, 39.6%) were not significantly difference in those of control zygotes (77.8%, 50.0%). Also, all of live-born young mice were chromosomally normal (n=40). This results suggested that proposed rapid vitrification procedures can be effectively use in 1-cell mouse zygotes cryopreservation.
Jo, Se-Hyun;Kim, Tae-Ho;Yu, Young-Bok;Oh, Jin-A;Jang, Mi-Hyang;Park, Ki-Moon
Korean Journal of Food Science and Technology
/
v.44
no.3
/
pp.350-355
/
2012
This study investigated the physiological effects of three species of Auricularia known as Auricularia polytricha (JNM21001), Auricularia auricula-judae black (JNM21002), and Auricularia auricula-judae brown (JNM21012). In the ORAC assay, Auricularia spp. showed antioxidant activities in the order of JNM21001>JNM21012>JNM21002. All Auricularia spp. strongly inhibited the action of ${\alpha}$-amyloglucosidase up to 60%. In order to further test in vivo anti-obesity effects, high fat diet induced ICR obese mice fed a diet containing 20% fat were used. All Auricularia spp. supplementation during high fat diet feeding significantly reduced body weight gain, epididymal fat pads weight, and lowered the food efficiency ratio compared to the high fat control (HFC) group. In particular, the group fed with JNM21012 had a lower average daily body weight gain of 0.45 g/day, demonstrating similar levels to the normal diet fed group. The group fed with JNM21012 significantly reduced lowered serum triglycerides (42%), total cholesterol (81%), and LDL-cholesterol level (66%) compared with the HFC group.
In this study, we designed to confirm the dietary effect of anti-obesity of fermented soybean curd residue (FSCR; SCR-Meju; Biji-meju) by A. oryzae, which is well known as a Korean traditional meju microbe. We observed that body weight gain, serum and hepatic lipid profile, as well as the activity of ROS generating enzyme and ROS scavenging enzyme in high-fat diet induced obese mice fed experimental diet (SCR and SCR-meju). Body weight gain and epididymal fat weight of HC (high-fat diet control) was markedly higher than that of NC (Normal control). Conversely, body weight gain and epididymal fat weight of the SCR (Biji) and SCR-meju (Biji-meju) group was significantly lower than that of HC; these of the SCR-meju group was lower than that of the SCR group. Furthermore, serum TG and total-cholesterol and LDL-cholesterol contents of SCR and SCR-meju groups were lower than that of HC, and HDL-cholesterol level of the SCR-meju group was significantly higher than that of HC. In conclusion, although precise mechanisms of the antiobese effects of SCR-meju in this study are unknown, the present study provides an experimental evidence that SCR-meju may prevent obesity and obesity related metabolic syndromes, such as hyperlipidemia, hypertension and diabetes, and liver disease by high-fat diet. Nevertheless, further study in this filed will be needed.
Growth differentiation factor-9 (GDF-9) is a member of the transforming growth factor $\beta$ (TGF-$\beta$) superfamily. It has been known that GDF-9 is a growth factor having a crucial role in normal folliculogenesis and its expression is oocyte-specific. The present study was aimed to elucidate the expression of GDF-9 mRNA in the mouse primordial follicles as well as in the other developmental stages. The semiquantitative analysis of GDF-9 mRNA expression was conducted. Total RNA was extracted from the ICR mice ovaries at gestational day 19, postnatal day 1, day 10, day 21, and day 28, and RT-PCR was performed to measure GDF-9 and $\beta$-actin mRNA levels. Level of GDF-9 mRNA were normalized against the level of $\beta$-actin mRNA, and compared among different stages. GDF-9 mRNA was detected in all samples including the fetal ovaries that mainly consists of primordial follicles. The highest level of mRNA was observed in ovaries obtained at day 10 that mainly consists of growing follicles. The present result suggests that GDF-9 may play an important role in the early stage of folliculogenesis.
This study was investigated on the antitumor of protein-polysaccharide fraction(PPF) extracted from seaweeds such as sea-staghorn and laver toward sarcoma-180 cells. In the PPF extracted from these sewaweeds, the polysaccharide contents of sea-staghorn and laver were $62.26\%$ and $65.78\%$, respectively. The highest levels of polysaccharides found in seaweeds was fructose. The major amino acids were aspartic acid, glutamic acid, glycine and cystein. The solid tumor growth inhibition showed the highest level of $53.30\%$ when 50mg/kg sea-staghorn was administrated. The life prolongation effect was $17.35\%$ at 50 mg/kg of laver. In the effects of immunologic activity, when 100mg/kg sea-staghorn was administrated, the number of circulating leucocyte showed the highest level of $82.23\%$ but decreased leucocyte for prolonged times. The number of total peritoneal exudate cells of the sea-staghorn administerated group was increased significantly in comparison with the control group. The hematobiolgoical analysis of the experimental group was similar with that of the control group. This experiments indicated that hemeastasis still maintained nor-mal state and not showed any harmful effects in normal mice.
Kim, Ha-Rim;Lee, Chang-Hyun;Jung, Mun Yhung;Kim, Jong-Seok;Kim, Hong-Jun;Jeon, Hye-Sook;Lee, Seung-Hyun;Kim, Ji-Hyun;Shin, Min-Ji;Ma, Sang-Yong;Kwon, Jin;Oh, Chan-Ho
Herbal Formula Science
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v.27
no.4
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pp.269-284
/
2019
This study was to investigate whether cultivated ginseng (CG), cultivated wild simulated ginseng (CWG) and cultivated red ginseng (CRG) extracts influences on the obesity. The saponin contents of 3 kinds of ginsengs were analysed by HPLC-ESI-TOF-MS. Total saponin contents were determined in CG on the most contents and since red ginseng has the highest PD (protopanaxadiol type) / PT (protopanaxatriol type) ratio, there may be differences between ginseng, wild ginseng, and red ginseng with respect to their pharmacological effects. Male C57BL/6J mice were fed a normal diet(N), HFD (60% Kcal fat, C), HFD with CG, CWG and CRG extracts (800 mg/kg) for 5 weeks. We observed change of total body weight, degree of hepatic lipid accumulation and immunohistochemical change of GLP-1 and insulin-secreting cells. Also this study attempts to use the physiological analysis method to analyze the changes of blood lipids, insulin and leptin concentration. The change of body weight and size of accumulated lipid droplets in liver lobules decreased in all of the experimental groups than the control(C) group. In the pancreas, the immunohistochemical density of insulin-secreting cells were significantly stronger in the CWG and CRG than C group. The levels of serum insulin and leptin significantly decreased 55.6%, 54.3% respectively in CWG and CRG. The changes of triglyceride, total cholesterol in serum decreased in CRG than the C group. Obesity related CG, CWG and CRG extracts might have contribute to improvement of obesity by regulating the levels of blood lipids and biochemical indicator of fat accumulation.
Background: The prevalence of allergic inflammatory diseases such as atopic dermatitis (AD), asthma, and allergic rhinitis worldwide has increased and complete recovery is difficult. Korean Red Ginseng, which is the heat-processed root of Panax ginseng Meyer, is widely and frequently used as a traditional medicine in East Asia. In this study, we investigated whether Korean Red Ginseng water extract (RGE) regulates the expression of proinflammatory cytokines and chemokines via the mitogen-activated protein kinases (MAPKs)/nuclear factor kappa B ($NF-{\kappa}B$) pathway in allergic inflammation. Methods: Compound 48/80-induced anaphylactic shock and 1-fluoro-2,4-dinitrobenzene (DNFB)-induced AD-like skin lesion mice models were used to investigate the antiallergic effects of RGE. Human keratinocytes (HaCaT cells) and human mast cells (HMC-1) were also used to clarify the effects of RGE on the expression of proinflammatory cytokines and chemokines. Results: Anaphylactic shock and DNFB-induced AD-like skin lesions were attenuated by RGE administration through reduction of serum immunoglobulin E (IgE) and interleukin (IL)-6 levels in mouse models. RGE also reduced the production of proinflammatory cytokines including $IL-1{\beta}$, IL-6, and IL-8, and expression of chemokines such as IL-8, thymus and activation-regulated chemokine (TARC), and macrophage-derived chemokine (MDC) in HaCaT cells. Additionally, RGE decreased the release of tumor necrosis $factor-{\alpha}$ ($TNF-{\alpha}$), $IL-1{\beta}$, IL-6, and IL-8 as well as expressions of chemokines including macro-phage inflammatory protein $(MIP)-1{\alpha}$, $MIP-1{\beta}$, regulated on activation, normal T cell expressed and secreted (RANTES), monocyte chemoattractant protein (MCP)-1, and IL-8 in HMC-1 cells. Furthermore, our data demonstrated that these inhibitory effects occurred through blockage of the MAPK and $NF-{\kappa}B$ pathway. Conclusion: RGE may be a useful therapeutic agent for the treatment of allergic inflammatory diseases such as AD-like dermatitis.
Phospholipase C-${\beta}$ (PLC-${\beta}$) hydrolyses phosphatidylinositol 4,5-bisphosphate and generates inositol 1,4,5-trisphosphate in response to activation of various G protein-coupled receptors (GPCRs). Using glial cells from knock-out mice lacking either PLC-${\beta}1$ [PLC-${\beta}1$ (-/-)] or PLC-${\beta}3$ [PLC-${\beta}3$ (-/-)], we examined which isotype of PLC-${\beta}$ participated in the cellular signaling events triggered by thrombin. Generation of inositol phosphates (IPs) was enhanced by thrombin in PLC-${\beta}1$ (-/-) cells, but was negligible in PLC-${\beta}3$ (-/-) cells. Expression of PLC-${\beta}3$ in PLC-${\beta}3$ (-/-) cells resulted in an increase in pertussis toxin (PTx)-sensitive IPs in response to thrombin as well as to PAR1-specific peptide, while expression of PLC-${\beta}1$ in PLC-${\beta}1$ (-/-) cells did not have any effect on IP generation. The thrombin-induced $[Ca^{2+}]_i$ increase was delayed and attenuated in PLC-${\beta}3$ (-/-) cells, but normal in PLC-${\beta}1$ (-/-) cells. Pertussis toxin evoked a delayed $[Ca^{2+}]_i$ increase in PLC-${\beta}3$ (-/-) cells as well as in PLC-${\beta}1$ (-/-) cells. These results suggest that activation of PLC-${\beta}3$ by pertussis toxin-sensitive G proteins is responsible for the transient $[Ca^{2+}]_i$ increase in response to thrombin, whereas the delayed $[Ca^{2+}]_i$ increase may be due to activation of some other PLC, such as PLC-${\beta}4$, acting via PTx-insensitive G proteins.
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