• Neonatal Medicine
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• v.17 no.2
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• pp.155-160
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• 2010

Metabolic acidosis is commonly encountered issues in the management of critically ill neonates and especially of preterm infants during early neonatal days. In extremely premature infants, low glomerular filtration rate and immaturity of renal tubules to produce new bicarbonate causes renal bicarbonate loss. Higher intake of amino acids, relatively greater contribution of protein to the energy metabolism and mineralization process in growing bones are also responsible for higher acid load in premature infant than in adult. Despite widespread use of sodium bicarbonate in the management of severe metabolic acidosis, use of sodium bicarbonate in premature infants should be restricted to a reasonable but unproven exception such as ongoing renal loss. Despite concern about the low pH value (<7.2) which can compromise cellular metabolic function, no treatment guideline has been established regarding the management of metabolic acidosis in premature infants. Appropriately powered randomized controlled trials of base therapy to treat metabolic acidosis in critically ill newborn infants are demanding.

• The Korean Journal of Food & Health Convergence
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• v.8 no.1
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• pp.17-20
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• 2022

Paralytic ileus is a metabolic state in which the intestines fail to transmit peristalsis due to failure of the neuromuscular mechanism in the small intestines and colon. It is a major cause of morbidity in hospitalized patients especially during late presentations and points of mismanagement. The causes include infections, electrolyte imbalance (hypokalemia, hyponatremia), surgeries and medications. When the exact cause of the disease condition is identified and corrected, paralytic ileus is usually resolved. This case report is that of a 16 year old female who was admitted and managed as a case of paralytic ileus. The patient presented with symptoms of fever, abdominal pain, abdominal distension, vomiting and inability to pass stool or flatus. There was associated body weakness, reduced urine output and weight loss. She was properly examined clinically and sent for various investigations. Investigations such plain abdominal X-Ray, serum electrolyte estimation, chest X-Ray and full blood count were carried out. The results of the investigations done were in keeping with the diagnosis of paralytic ileus, electrolyte imbalance and ongoing sepsis. She was subsequently managed through nil per oral, adequate fluid rehydration, antibiotics and correction of electrolyte imbalance. Following stable clinical state and investigation results, she was discharged and advised on follow-up.

• Clinical Nutrition Research
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• v.13 no.2
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• pp.121-129
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• 2024

The prevalence of metabolic syndrome caused by diets containing excessive fatty acids is increasing worldwide. Patients with metabolic syndrome exhibit abnormal lipid profiles, chronic inflammation, increased levels of saturated fatty acids, impaired insulin sensitivity, excessive fat accumulation, and neuropathological issues such as memory deficits. In particular, palmitic acid (PA) in saturated fatty acids aggravates inflammation, insulin resistance, impaired glucose tolerance, and synaptic failure. Recently, adiponectin, brain-derived neurotrophic factor (BDNF), and glucose-like peptide-1 (GLP-1) have been investigated to find therapeutic solutions for metabolic syndrome, with findings suggesting that they are involved in insulin sensitivity, enhanced lipid profiles, increased neuronal survival, and improved synaptic plasticity. We investigated the effects of adiponectin, BDNF, and GLP-1 on neurite outgrowth, length, and complexity in PA-treated primary cortical neurons using Sholl analysis. Our findings demonstrate the therapeutic potential of adiponectin, BDNF, and GLP-1 in enhancing synaptic plasticity within brains affected by metabolic imbalance. We underscore the need for additional research into the mechanisms by which adiponectin, BDNF, and GLP-1 influence neural complexity in brains with metabolic imbalances.

• Journal of Veterinary Clinics
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• v.9 no.2
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• pp.467-472
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• 1992

Seven patients with signs of metabolic bone disease clinically seen at the Veterinary Teaching Hospital of Seoul National University from May 1990 to February 1992 were evaluated retrospectively. 1. Clinical signs include bowed leg, deformity of spine, digestive disturbance, constipation, retarded growth, lameness and hindlimb paralysis. 2. Radiographical sings include generalized skeletal demineralization, decreased radiological contrast between skeleton and soft tissues, thinning of bone cortex and pathological fractures. The diagnosis of nutritional secondary hyperparathyroidism resulting in metabolic bone disease caused by mineral imbalance was made based upon history, clinical signs, physical examination and radiographical signs.

• Molecules and Cells
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• v.38 no.8
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• pp.677-684
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• 2015

Osteoarthritis (OA) is one of the most prevalent forms of joint disorder, associated with a tremendous socioeconomic burden worldwide. Various non-genetic and lifestyle-related factors such as aging and obesity have been recognized as major risk factors for OA, underscoring the potential role for epigenetic regulation in the pathogenesis of the disease. OA-associated epigenetic aberrations have been noted at the level of DNA methylation and histone modification in chondrocytes. These epigenetic regulations are implicated in driving an imbalance between the expression of catabolic and anabolic factors, leading eventually to osteoarthritic cartilage destruction. Cellular senescence and metabolic abnormalities driven by OA-associated risk factors appear to accompany epigenetic drifts in chondrocytes. Notably, molecular events associated with metabolic disorders influence epigenetic regulation in chondrocytes, supporting the notion that OA is a metabolic disease. Here, we review accumulating evidence supporting a role for epigenetics in the regulation of cartilage homeostasis and OA pathogenesis.

• Journal of Obesity & Metabolic Syndrome
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• v.27 no.4
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• pp.254-261
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• 2018

Background: The most beneficial dietary pattern in managing metabolic syndrome (MetS) in the elderly has not been ascertained. The aim of this study is to classify dietary patterns and to examine associations between dietary pattern, MetS and body composition in elderly Koreans. Methods: This study was conducted among Koreans 65 years or older using data from the Korea National Health and Nutrition Examination Survey in 2009. A total of 1,567 study subjects were included. All statistical analyses were conducted using SPSS version 20.0 and dietary patterns were classified by cluster analysis. Results: There were three dietary patterns derived by cluster analysis in this study. We observed that most South Korean elderly still maintain a traditional dietary pattern. Dietary patterns were classified as balanced (31%), imbalanced (40%), or very imbalanced (30%), with the majority of subjects having an unbalanced diet pattern in which their total energy and nutrient intake was insufficient compared with the Dietary Reference Intake for Koreans. Those in the very imbalanced group had a ratio of macronutrients (carbohydrates:fats:protein) of 81.15:7.18:11.50 and a 54% higher likelihood of having hypertriglyceridemia (P=0.025) compared with those in the balanced group. Conclusion: The current findings indicate that the diets of South Korean elderly are nutritionally imbalanced, including high carbohydrate consumption, which confers a high risk hypertriglyceridemia. These findings highlight the effect of nutritional imbalance in elderly with MetS.

• Journal of Microbiology and Biotechnology
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• v.30 no.12
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• pp.1937-1943
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• 2020

Although classical metabolic engineering strategies have succeeded in developing microbial strains capable of producing desired bioproducts, metabolic imbalance resulting from extensive genetic manipulation often leads to decreased productivity. Thus, abiotic strategies for improving microbial production performance can be an alternative to overcome drawbacks arising from intensive metabolic engineering. Herein, we report a promising abiotic method for enhancing lycopene production by UV-C irradiation using a radiation-resistant ΔcrtLm/crtB+dxs+ Deinococcus radiodurans R1 strain. First, the onset of UV irradiation was determined through analysis of the expression of 11 genes mainly involved in the carotenoid biosynthetic pathway in the ΔcrtLm/crtB+dxs+ D. radiodurans R1 strain. Second, the effects of different UV wavelengths (UV-A, UV-B, and UV-C) on lycopene production were investigated. UV-C irradiation induced the highest production, resulting in a 69.9% increase in lycopene content [64.2 ± 3.2 mg/g dry cell weight (DCW)]. Extended UV-C irradiation further enhanced lycopene content up to 73.9 ± 2.3 mg/g DCW, a 95.5% increase compared to production without UV-C irradiation (37.8 ± 0.7 mg/g DCW).

• The Korean Journal of Emergency Medical Services
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• v.25 no.1
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• pp.243-249
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• 2021

A decrease in coronary blood flow leads to an imbalance between the supply of oxygen to the myocardium and its demand, and reversible or irreversible damage to the myocardium could occur depending on the severity of the resultant ischemia and the duration of the imbalance. This imbalance results in a cascade of ischemic reactions in the following order: metabolic abnormalities, diastolic dysfunction, systolic dysfunction, and electrocardiogram changes. Variant angina is caused by the closure of the coronary artery due to reversible coronary artery spasm, resulting in myocardial ischemia and subsequent chest pain as a clinical symptom. Variant angina may be observed as ST segment elevation in electrocardiogram measured when present in chest pain. However, 12-lead electrocardiogram performed after the patient's chest pain resolves does not help in the diagnosis. Since the duration of chest pain appears to be <15 minutes, it is important to perform the 12-lead electrocardiogram when clinical symptoms are present. If nitroglycerin is administered without performing 12-lead electrocardiogram by 119 pre-hospital paramedics, the chest pain would be resolved, making it impossible to identify changes in the ST segment. Before administration of nitroglycerin, changes in the ST segment must be recorded by performing 12-lead electrocardiogram.

• Applied Biological Chemistry
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• v.43 no.4
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• pp.236-240
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• 2000

Correlations between mitochondrial respiration, glycolysis activity and overall growth activity of rice (Oryza sativa: cv. Dasan) seedlings during low temperature exposure were studied in order to provide insights into the underlying mechanism for the primary phase of chilling injury in plants. Among cellular membranes involved in energy metabolism, only the mitochondrial inner membrane showed not only physical phase transition at ca. $13^{\circ}C$, as monitored by ESR spin label, but also functional phase transition at the same temperature, as assessed by cytochrome c oxidase activity. The main regulatory enzyme of glycolysis, phosphofructokinase, in situ did not suffer phase transition of its activity at least in the $4{\sim}27^{\circ}C$ range. Low temperature caused a significant accumulation of glucose 6-phosphate (G6P) and fructose 6-phosphate (F6P), which disappeared almost completely on rewarming of the seedlings. Temperature profiles of the steady state levels of G6P and F6P revealed the inflection point appearing at around phase transition temperature of the mitochondrial membrane. The results conform to our previous proposition on the mechanism for the early stage events of chilling injury that the accumulation of glycolytic metabolites in cells due to metabolic imbalance at low temperature gives rise to an excess supply of electrons during rewarming period, which, in turn, results in overproduction of active oxygen in mitochondria.

• Journal of The Korean Society of Inherited Metabolic disease
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• v.2 no.1
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• pp.15-19
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• 2002

Disorders resulting from defects in peroxisomal biogenesis include Zellweger syndrome, neonatal adrenoleukodystrophy, and infantile Refsum disease. The three diseases are now considered as a continuum of clinical features. Neonatal adrenoleukodystrophy is intermediate between Zellweger syndrome and infantile Refsum disease in severity, and is characterized by profound hypotonia, intractable seizures and premature death. We report a cases of neonatal adrenoleukodystrophy presenting with neonatal seizure and hypotonia. At the age of 43 months, she had clinical evidence of adrenal insufficiency with skin hyperpigmentation and electrolyte imbalance. She was diagnosed having neonatal adrenoleukodystrophy based on abnormally high levels of plasma very long-chain fatty acids, pipecolic acid and phytanic acid.