• Asian-Australasian Journal of Animal Sciences
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• v.22 no.7
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• pp.1005-1015
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• 2009

Two experiments were carried out to determine the utility of sainfoin hay, a temperate tanniferous forage legume, as a dietary supplement for grass-fed cows. The condensed tannins (CT) of sainfoin might counteract the typical metabolic ammonia load of cows in intensive grazing systems. Furthermore, the physical fibrousness of sainfoin might improve ruminal pH stability. In the preliminary experiment, the eating rate of non-lactating Holstein cows of two tanniferous hays, sainfoin and birdsfoot trefoil, was compared to that of a grass-clover hay after specific periods of time (n = 4). The eating rate of sainfoin was superior to that of the other forages. In the main experiment, designed as a replicated 3${\times}$3 Latin square, six ruminally-cannulated, lactating Red Holstein cows received grass, concentrate and either no supplementation, 3 kg/d of grass hay or 3 kg/d of sainfoin hay (n = 6). Measured intakes of the grass hay and the sainfoin hay were 2.0 and 1.5 kg DM, and two cows entirely refused to eat the sainfoin hay and had to be excluded from data analysis. Grass DMI was similar for cows supplemented with sainfoin hay and cows fed only grass whereas intake of concentrate was higher (p<0.01) for the latter treatment. Continuous measurement of ruminal pH showed that the minimum pH at night tended to be lower (p<0.10) with grass-only feeding compared to sainfoin supplementation, but pH did not decline below the threshold of subacute acidosis for a longer period of time. The slightly higher intake of nitrogen (N) for cows supplemented with sainfoin hay (413 g/d) compared to cows fed only grass (399 g/d) was accompanied by an increased (p<0.05) fecal N excretion and a tendency for an increased (p<0.10) urinary N excretion. Ruminal ammonia concentration, as well as plasma and milk urea, were not affected by sainfoin supplementation. In conclusion, the lack of positive effects typical for CT might be explained either by the limited CT content of this plant species (55 g/kg DM) or the relatively low proportion of sainfoin in the total diet or both. Moreover, due to the unexpected low grass quality, the general ammonia load might have been too low for CT to have an impact.

• Maxillofacial Plastic and Reconstructive Surgery
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• v.19 no.1
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• pp.109-114
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• 1997

Malignant hyperthermia is a hypermetabolic, fatal syndrome triggered by anesthetic drugs that occurs frequently in genetically susceptible persons. It is characterized by tachycardia, rapidly increasing temperature, skeletal muscle rigidity, respiratory and metabolic acidosis, cyanosis etc. It has been noted that the majority of cases of malignant hyperthermia are fatal unless early diagnosis and treatment are performed. Thus, the accurate prediction of preanesthetic susceptibility and early diagnosis of malignant hyperthermia is necessary to appropriate treatment. Dantrolene sodium has been shown to be effective in the prevention and treatment of malignant hyperthermia. We experienced a case of malignant hyperthermia, which is presented of a 32-year-old healthy male patient in whom a orthognatic surgery was performed under $O_2-N_2O$-enfl-rane anesthesia with induction by pentobarbital and succinylcholine. We discuss this case with reviewing the history, incidence, etiology, pathophysiology, clinical signs & biochemical changes, prevention & treatment.

• Childhood Kidney Diseases
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• v.14 no.2
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• pp.132-142
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• 2010

Hypokalemia usually reflects total body potassium deficiency, but less commonly results from transcellular potassium redistribution with normal body potassium stores. The differential diagnosis of hypokalemia includes pseudohypokalemia, cellular potassium redistribution, inadequate potassium intake, excessive cutaneous or gastrointestinal potassium loss, and renal potassium wasting. To discriminate excessive renal from extrarenal potassium losses as a cause for hypokalemia, urine potassium concentration or TTKG should be measured. Decreased values are indicative of extrarenal losses or inadequate intake. In contrast, excessive renal potassium losses are expected with increased values. Renal potassium wasting with normal or low blood pressure suggests hypokalemia associated with acidosis, vomiting, tubular disorders or increased renal potassium secretion. In hypokalemia associated with hypertension, plasam renin and aldosterone should be measured to differentiated among hyperreninemic hyperaldosteronism, primary hyperaldosteronism, and mineralocorticoid excess other than aldosterone or target organ activation. Hypokalemia may manifest as weakness, seizure, myalgia, rhabdomyolysis, constipation, ileus, arrhythmia, paresthesias, etc. Therapy for hypokalemia consists of treatment of underlying disease and potassium supplementation. The evaluation of hyperkalemia is also a multistep process. The differential diagnosis of hyperkalemia includes pseudohypokalemia, redistribution, and true hyperkalemia. True hyperkalemia associated with decreased glomerular filtration rate is associated with renal failure or increased body potassium contents. When glomerular filtration rate is above 15 mL/min/$1.73m^2$, plasma renin and aldosterone must be measured to differentiate hyporeninemic hypoaldosteronism, primary aldosteronism, disturbance of aldosterone action or target organ dysfunction. Hyperkalemia can cause arrhythmia, paresthesias, fatigue, etc. Therapy for hyperkalemia consists of administration of calcium gluconate, insulin, beta2 agonist, bicarbonate, furosemide, resin and dialysis. Potassium intake must be restricted and associated drugs should be withdrawn.

• Journal of The Korean Society of Inherited Metabolic disease
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• v.14 no.2
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• pp.123-134
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• 2014

Recent advances in the diagnosis and treatment of inborn errors of metabolism (IEM) have improved substantially the prognosis of many of these diseases, if diagnosed early enough before irreversible damage occurs. Diseases of inborn errors of metabolism are so diverse over several hundred disease up to now and may be several thousand in near future, and these diversities of IEMs make clinicians embarassed. The signs of neurological dysfunctions of many IEMs manifesting in the neonatal period is very nonspecific, such as poor feeding, poor sucking, apnea or tachypnea, vomiting, hypertonia, hypotonia, seizure, letharginess, consciousness change and coma. But after neonatal period, the signs of neurological deficits become specific and localized. The results of routine basal laboratory tests such as metabolic acidosis, hyperammonemia, lactic acidemia, ketonemia or hyperuricemia can give very important clinical clues for the diagnosis of IEMs. Even no abnormal findings on routine laboratory test could be very important clue for NKH, sulfite oxidase deficiency and peroxisomal disorders. These various clinical manifestations of these diverse diseases can be categorized and summarized. This makes it essential that the practicing clinicians be familiar with the clinical presentations and symptomatic and systematic approaches of these disorders. Characteristic clinical presentations, methods of symptomatic and systematic approach and typing of various disorders is discussed in this review.

• Pediatric Gastroenterology, Hepatology & Nutrition
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• v.9 no.2
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• pp.153-161
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• 2006

Purpose: This study was designed to investigate rotavirus infection by comparing the clinical characteristics in neonates and infants. Methods: We enrolled 104 neonates and 250 infants wiht gastroenteritis and a rotazyme test positive reaction at the Soonchunhyang University Bucheon Hospital from February 2001 to January 2003. Results: The seasonal peaks of infection in infants occurred from February to June. However, in neonates, it occurred from October to December due to nursery outbreaks. Diarrhea, vomiting, fever and convulsions were significant symptoms in infants; however, metabolic acidosis with dehydration, jaundice, irritability, apnea, bloody stool, gastric residual, grunting, poor oral intake, lethargy as well as fever and diarrhea were more common in the neonates. Upper respiratory infection, pneumonia and bronchitis were present in the infants; however, necrotizing enterocolitis was more commonly observed in the in neonates. Among the patients with rotaviral infection, formula feeding was more popular than breast milk feeding in both the neonates and infants; however, this finding was not statistically significant. Conclusion: Rotavirus can be a significant pathogen in neonates as well as infants. Neonates suffering from fever, poor oral intake, lethargy and apnea should be investigated for rotaviral infection. A new vaccine, rotaviral specific immunoglobulin and treatment guidelines are needed for eradicating rotavirus infection. Further studies on isolation, infection pathway, immune response and treatment of rotavirus are needed.

• Journal of Chest Surgery
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• v.45 no.4
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• pp.236-241
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• 2012

Background: Prolonged usage of extracorporeal membrane oxygenation (ECMO) may induce multi-organ failure. This study is aimed to evaluate prognostic factors in the patients with ECMO. Also, the prognosis of ECMO with Kidney Injury Network Scoring system is studied. Materials and Methods: From May 2005 to July 2011, 172 cases of ECMO were performed. The cases of perioperative use of ECMO were excluded. Renal failure patient and younger than 15 years old one were also excluded. As a result, 26 cases were enrolled in this study. Male patients were 15 (57.7%), and mean age was $56.57{\pm}17.03$ years old. Demographic data, ECMO parameters, weaning from ECMO, and application of continuous renal replacement therapy are collected and Acute Kidney Injury Network (AKIN) scores were evaluated just before ECMO and day 1, day 2 during application of ECMO. Results: Venoarterial ECMO was applied in 22 cases (84.6%). The reasons for applications of ECMO were cardiac origin in 21 (80.8%), acute respiratory distress syndrome in 4, and septic shock in 1 case. Successful weaning from ECMO was achieved in 15 cases (57.7%), and survival discharge rate was 9 cases (34.6%). Mean duration of application of ECMO was $111.39{\pm}54.06$ hours. In univariate analysis, myocarditis was independent risk factors on weaning failure. Using the receiver operating characteristic curve, level of hemoglobin on 24 hours after ECMO, and base excess on 48 hours after ECMO were showed more than 0.7. AKIN score was not matched the prognosis of the patients with ECMO. Conclusion: In our study, the prognosis of the patients with myocarditis was poor. Hemoglobin level at first 24 hours, and degree of acidosis at 48 hours were useful methods in relating with prognosis of ECMO. AKIN scoring system was not related with the prognosis of the patients. Further study for prognosis and organ injury during application ECMO may be needed.

• Journal of The Korean Society of Inherited Metabolic disease
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• v.15 no.1
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• pp.35-39
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• 2015

Medium-chain acyl-CoA dehydrogenase (MCAD) deficiency is the most common mitochondrial fatty acid oxidation disorder which is inherited as an autosomal recessive pattern. MCAD deficiency is caused by mutations in the ACADM gene; medium-chain acyl-CoA dehydrogenase gene (ACADM; OMIM 607008) on chromosome 1p31 which encodes MCAD, the mitochondrial enzyme which catalyzes the first reaction in beta-oxidation of fatty acids with medium-chain length. Here, we describe one Korean pediatric case of MCAD deficiency, which was diagnosed during newborn screening by tandem mass spectrometry and confirmed by molecular analysis. The level of hexanoyl (C6), octanoyl (C8), decenoyl (C10:1) carnitine, and C8/C2 ratio was elevated. Homogenous c.1189T>A (p.Tyr397Asn) mutation of ACADM gene was identified by direct sequencing. He has been asymptomatic and has shown normal growth and development by 25 months of age without any intervention. There was no episode of metabolic acidosis during follow-up period.

• Journal of The Korean Society of Inherited Metabolic disease
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• v.15 no.1
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• pp.18-24
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• 2015

Glycogen storage disease type Ib (GSD Ib) is one of the rare inherited metabolic disease caused by mutation of SLC37A4 gene. Clinical characteristics include hepatomegaly, hypoglycemia, lactic acidosis, hyperlipidemia and high serum uric acid concentration. The authors analyzed clinical and molecular characteristics of three Korean patients (one male and two females) with GSD Ib by retrospective review of medical records. Two patients were diagnosed in toddler period by hypoglycemia and hepatomegaly. One patient was diagnosed by growth retardation and short stature in puberty. c.412T>C (p.Trp138Arg) (3/6 alleles, 50.0%) was most frequently observed, following by p.Leu348Valfs*53 (1 allele), p.Pro191Leu (1 allele), p.Ala148Val (1 allele) in molecular analysis. Uncooked corn starch and allopurinol was administered. Because all three patients had neutropenia and recurrent infections, G-CSF was administered. Two patients had severe osteoporosis needing calcium supplement. The patient who diagnosed at puberty had relatively poor prognosis demonstrated by having severe infection and complications in liver and kidney.

• Journal of The Korean Society of Inherited Metabolic disease
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• v.15 no.1
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• pp.9-17
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• 2015

Glycogen storage disease (GSD) type Ia is rare inborn metabolic disorder, caused by glucose-6-phosphatase deficiency. It characterized by hepatomegaly, hypoglycemia, lactic acidosis, hypertriglyceridemia, and hyperuricemia and it is usually manifested in the infantile period. In addition, it is also associated with growth failure, pubertal delay, anemia, platelet dysfunction, osteopenia, and pulmonary hypertension. Hepatocellular adenoma and renal dysfunction are frequent late complications. Delayed diagnosis and inappropriate therapy lead to many complications such as growth failure, osteoporosis, refractory gout, renal failure, hepatocellular carcinoma (HCC), and pulmonary hypertension. Here, two Korean sisters diagnosed with GSD Ia, aged 33 and 36 respectively, were described and compared to recent articles about four adults with late diagnosis of GSD Ia. One sister had typical manifestations of GSD Ia including short stature (height, 145 cm), multiple hepatic adenoma, chronic kidney disease stage IV, and severe osteoporosis, whereas the older sister had normal stature (162 cm), one tiny hepatic nodule, and normal renal function. Direct sequencing of G6PC in two sisters identified a homozygous splicing mutation, c.645G>T, which is a prevalent mutation in Korea. Interestingly, our cases and four adults from recent reports had asymptomatic mild hypoglycemia and various manifestations including renal failure, HCC, fatty liver, or uncontrolled hyperlipidemia. These adult cases represent not only heterogenous phenotype to genotype within family members with GSD Ia but also long-term complications such as gouty arthritis, renal failure, and osteoporosis in untreated adult GSD Ia patients. In addition, lactic academia and hypertriglyceridemia are good markers of GSD Ia to distinguish from metabolic disease.

• Journal of Radiation Protection and Research
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• v.43 no.2
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• pp.66-74
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• 2018

Background: Tumor response to anticancer therapies can much be influenced by microenvironmental factors. In this study, we determined the effect of these microenvironmental factors on DNA methylation using A549 human lung adenocarcinoma cell line. Materials and Methods: We subjected A549 cells to various conditions mimicking tumor microenvironment including hypoxia, acidosis (sodium lactate), oxidative stress ($H_2O_2$), bystander effect (supernatant from doxorubicin (Dox)-treated or irradiated cells), and immune cell infiltration (supernatant from THP-1 or Jurkat T cells). Genomic DNA was isolated from these cells and analyzed for DNA methylation. Clonogenic cell survival, gene expression, and metabolism were analyzed in cells treated with some of these conditions. Results and Discussion: We found that DNA methylation level was significantly decreased in A549 cells treated with conditioned media from Dox-treated cells or Jurkat T cells, or sodium lactate, indicating an active transcription. To determine whether the decreased DNA methylation affects radiation sensitivity, we exposed cells to these conditions followed by 6 Gy irradiation and found that cell survival was significantly increased by sodium lactate while it was decreased by conditioned media from Dox-treated cells. We further observed that cells treated with conditioned media from Dox-treated cells exhibited significant changes in expression of genes including BAX and FAS (involved in apoptosis), NADPH dehydrogenase (mitochondria), EGFR (cellular survival) and RAD51 (DNA damage repair) while sodium lactate increased cellular metabolism rather than changing the gene expression. Conclusion: Our results suggest that various tumor microenvironmental factors can differentially influence DNA methylation and hence radiosensitivity and gene expression in A549 cancer cells.