• Tuberculosis and Respiratory Diseases
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• v.44 no.3
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• pp.583-591
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• 1997

The functional derangement of skeletal muscles which may be attributed to chronic hypoxia has been accepted as a possible mechanism of exercise impairment in patients with chronic obstructive pulmonary disease (COPD). The metabolic changes in skeletal muscle in patients with COPD are characterized by impaired oxidative phosphorylation, early activation of anaerobic glycolysis and excessive lactate and hydrogen ion production with exercise. But the cause of exercise limitation in patients with chronic lung disease without hypoxia has not been known. In order to evaluate the change in the skeletal muscle metabolism as a possible cause of the exercise limitation in chronic lung disease patients without hypoxia, we compared the muscular metabolic data of seven male patients which had been derived from noninvasive $^{31}P$ magnetic resonance spectroscopy(MRS) with those of five age-matched normal male control persons. $^{31}P$ MRS was studied during the sustained isometric contraction of the dominant forearm flexor muscles up to the exhaustion state and the recovery period. Maximal voluntary contraction(MVC) force of the muscle was measured before the isometric exercise, and the 30% of MVC force was constantly loaded to each patient during the isometric exercise. There were no differences of intracellular pH (pHi) and inorganic phosphate/phosphocreatine(Pi/PCr) at baseline, exhaustion state and recovery period between two groups. But pHi during the exercise was lower in patients group than the control group (p < 0.05). Pi/PCr during the exercise did not show significant difference between two groups. These results suggest that the exercise limitation in chronic lung disease patients without hypoxia also could be attributed to the abnormalities in the skeletal muscle metabolism.

• Maxillofacial Plastic and Reconstructive Surgery
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• v.23 no.1
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• pp.1-6
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• 2001

Purpose : This study was undertaken to observe the occurrence of the vessel aneurysms according to several different methods of microvascular anastomosis. Mterials & methods : Forty Sprague-Dawley rats, weighing $180{\sim}200$ grams, were used for this experiment. The rats were divided into 4 groups. Group 1 (10 rats): The adventitia was trimmed off 5mm from the cut edge each and 20 arterial anastomoses were performed using 8 to 10 interrupted 9-0 polypropylene ($Prolene^{TM}$, Ethicon, U.K.) suture. Group 2 (10 rats): The adventitia was trimmed off as in group 1. Twenty arterial anastomoses were performed using continuous 9-0 polypropylene($Prolene^{TM}$, Ethicon, U.K.) suture. Group 3 (10 rats): The adventitia was stripped only 1mm from the cut edge each but not removed,. Twenty arterial anastomoses were performed using 8 to 10 interrupted 9-0 polypropylene($Prolene^{TM}$, Ethicon, U.K.) suture. Group 4 (10 rats): The adventitia was handled as in group 3. Twenty arterial anastomoses were performed using 9-0 polypropylene($Prolene^{TM}$, Ethicon, U.K.) suture. The arteries of the animals in all groups were explored at 28th days. We examined patency, presence of an aneurysm, other vascular abnormalities and microscopically observed the aneurysms with H&E and Van-Gieson stains. Result : 1. Patency rate was 80% in group 1, 95% in group 2, 85% in group 3 and 90% in group 4, respectively. 2. Aneurysm occurred 20% in group 1, 5% in group 2, 5% in group 3 and 5% in group 4, respectively. 3. There was no other vascular abnormalities in each group. 4. Infection rate was 5% in group 1, 0% in group 2, 20% in group 3 and 15% in group 4, respectively. 5. In the histopathological findings, we observed partially necrotic changes, loss and fragmentation of outer elastic lamella of smooth muscle in media and the proliferation of hyperplastic subintima. A lot of inflammatory cells were infiltrated in hyperplastic intima. Conclusions : On the basis of these observation, we could state that there were little differences in the occurrence of aneurysms according to different anastomotic suture methods.

• Pediatric Gastroenterology, Hepatology & Nutrition
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• v.4 no.2
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• pp.249-255
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• 2001

Methylmalonic acidemia is a rare congenital autosomal recessive metabolic disease. It is caused by blocking in the pathways of isoleucine, valine, threonine, methionine, cholesterol and odd-chain fatty acids to succinyl CoA, resulting in the increase of L-methylmalonyl CoA and methylmalonic acid. In most cases, there are symptoms such as recurrent vomitings, lethargy and laboratory abnormalities including metabolic acidosis and hyperammonemia from the neonatal period. We had a 6-month-old infant with methylmalonyl acidemia who presented with recurrent vomiting episodes since 3 months of age, failure to thrive and developmental delay. The laboratory findings showed hyperammoninemia and ketotic metabolic acidosis. Plasma amino acid analysis showed nonspecific finding. Urine organic acid ananysis by gas chromatography and mass spectrometry detected large amount of methylmalonic acid excreted in the urine. We restrained the supply of protein in the amount of 1~1.5 g/kg of body weight a day using leucine, isoleucine and valine-r-estrained milk and administered vitamine $B_{12}$, in the amount of 1mg per day. During the follow-up in the outpatient clinic, He could control his head and showed increased muscle strength.

• IMMUNE NETWORK
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• v.11 no.3
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• pp.135-154
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• 2011

The great discovery of microRNAs (miRNAs) has revolutionized current cell biology and medical science. miRNAs are small conserved non-coding RNA molecules that post-transcriptionally regulate gene expression by targeting the 3' untranslated region of specific messenger RNAs for degradation or translational repression. New members of the miRNA family are being discovered on a daily basis and emerging evidence has demonstrated that miRNAs play a major role in a wide range of developmental process including cell proliferation, cell cycle, cell differentiation, metabolism, apoptosis, developmental timing, neuronal cell fate, neuronal gene expression, brain morphogenesis, muscle differentiation and stem cell division. Moreover, a large number of studies have reported links between alterations of miRNA homeostasis and pathological conditions such as cancer, psychiatric and neurological diseases, cardiovascular disease, and autoimmune disease. Interestingly, in addition, miRNA deficiencies or excesses have been correlated with a number of clinically important diseases ranging from cancer to myocardial infarction. miRNAs can repress the gene translation of hundreds of their targets and are therefore well-positioned to target a multitude of cellular mechanisms. As a consequence of extensive participation in normal functions, it is quite logical to ask the question if abnormalities in miRNAs should have importance in human diseases. Great discoveries and rapid progress in the past few years on miRNAs provide the hope that miRNAs will in the near future have a great potential in the diagnosis and treatment of many diseases. Currently, an explosive literature has focussed on the role of miRNA in human cancer and cardiovascular disease. In this review, I briefly summarize the explosive current studies about involvement of miRNA in various human cancers and cardiovascular disease.

• The Journal of Korean Academy of Prosthodontics
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• v.56 no.1
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• pp.31-39
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• 2018

The collapse of the posterior occlusion destroys the normal occlusal plane and causes excessive wear reducing the vertical dimension. Reduced vertical dimension of occlusion causes not only aesthetic and functional problems but also overloading on the temporomandibular joints and abnormalities of muscle nerve system. In order to improve the collapsed occlusal relationship, it is necessary to consider the change of the vertical dimension. It is necessary to make a precise diagnosis and analysis before the treatment and to evaluate the adaption of patient to the new vertical dimension of occlusion. A patient with excessive overbite often has occlusal problems of tooth wear and tooth eruption. Considering these considerations, overall prosthodontic restoration is required to solve the problem. A patient of 68 year old man in this case who suffered major tooth wear and maxillary posterior teeth loss was treated with elevation of vertical dimension of occlusion by maxillary removable dental prosthesis and mandibular fixed prosthesis.

• Journal of Korean Neurosurgical Society
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• v.58 no.5
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• pp.412-418
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• 2015

Objective : To investigate the effects of posterior implant rigidity on spinal kinematics at adjacent levels by utilizing a cadaveric spine model with simulated physiological loading. Methods : Five human lumbar spinal specimens (L3 to S1) were obtained and checked for abnormalities. The fresh specimens were stripped of muscle tissue, with care taken to preserve the spinal ligaments and facet joints. Pedicle screws were implanted in the L4 and L5 vertebrae of each specimen. Specimens were tested under 0 N and 400 N axial loading. Five different posterior rods of various elastic moduli (intact, rubber, low-density polyethylene, aluminum, and titanium) were tested. Segmental range of motion (ROM), center of rotation (COR) and intervertebral disc pressure were investigated. Results : As the rigidity of the posterior rods increased, both the segmental ROM and disc pressure at L4-5 decreased, while those values increased at adjacent levels. Implant stiffness saturation was evident, as the ROM and disc pressure were only marginally increased beyond an implant stiffness of aluminum. Since the disc pressures of adjacent levels were increased by the axial loading, it was shown that the rigidity of the implants influenced the load sharing between the implant and the spinal column. The segmental CORs at the adjacent disc levels translated anteriorly and inferiorly as rigidity of the device increased. Conclusion : These biomechanical findings indicate that the rigidity of the dynamic stabilization implant and physiological loading play significant roles on spinal kinematics at adjacent disc levels, and will aid in further device development.

• The Journal of the Korea Contents Association
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• v.10 no.10
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• pp.237-245
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• 2010

Nerve conduction studies (NCS) are the most objective measure of nerve function and essential for the diagnosis of sub-clinical neuropathy in diabetes mellitus and diabetic polyneuropathy (DPN). This study evaluates the characteristic of electrophysiological abnormalities in DPN. Electrodiagnostic data from 120 patients with diabetic polyneuropathies and 77 control subjects were reviewed. Motor nerve conduction velocities (MNCV), distal motor latencies (DML), compound muscle action potential (CMAP) amplitudes, No potential frequency and conduction block were analyzed. Data were normalized based on normative reference values, and the proportion of nerves with abnormal values in the lower and upper limbs were evaluated. DPN was systemic demyelinating peripheral polyneuropathy and more severe abnormal nerve conduction was found in lower limbs than in upper limbs. The abnormal degree was more severe in peroneal nerve. It was no statistically significant difference of conduction block in control and DPN group. Our findings suggest that DPN had more common and severe peroneal nerve involvement in the motor nerve conduction studies (MNCS). These findings have important implications for the electrophysiological evaluation of DPN.

• Journal of Science and Technology Studies
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• v.14 no.1
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• pp.87-116
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• 2014

This article focuses on synthetic hormone consumption that illegal act of heterogeneous forms of pharmaceuticalization. Athletes are not unfamiliar with the use of synthetic hormones that contain anabolic steroids. Synthetic hormones are used to increase muscle mass and strength. This drug use practice cannot simply be viewed as illegal. Athletes accumulate knowledge on these hormones that conflicts with the knowledge proffered by physicians and they consume drugs responsibly. Physicians' knowledge of these hormones is limited to their use in the treatment of abnormalities. Athletes, however, are expanding the role of these hormones to include their potential for enhancement. Thereby, a new value is assigned to synthetic hormones, and an informal market is formed. Previous studies in the fields of biopolitics and biomedicalization have mainly focused on the formal connection between biomedical science and the institutional network. This article, therefore, analyzes the informal and the various aspects of biomedicalization.

• Journal of Chest Surgery
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• v.34 no.7
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• pp.552-555
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• 2001

Noonan syndrome is characterized by a Turner-like phenotype and a normal karyotype associated with congenital abnormalities, such as short stature, variable mental retardation, hypertelorism, webbed neck, low posterior hair line, skeletal malformation and congenital cardiovascular defect. Two third of Noonan syndrome have cardiac anormalies, half with pulmonary stenosis. We have experienced two cases of pulmonary stenosis associated with other cardiac anomalies in Noonan syndrome. The first 31-year-old male patient had characteristic appearance of Noonan syndrome with severe infundibular pulmonic stenosis and patent foramen ovate. The second 28-year-old male patient had valvular and subvalvular Pulmonary stenosis with typical Noonan\`s face and stature. Pulmonary valvotomy and hypertrophied muscle bundles in the right ventricular cavity were resected in both cases. Patent foramen ovate was closed directly in the first case. Postoperative follow-up examinations revealed no symptoms and successful outcome.

• Asian-Australasian Journal of Animal Sciences
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• v.31 no.11
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• pp.1795-1806
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• 2018

Objective: The study was designed to establish choline deficiency model (CDM) in broilers for evaluating efficacy of polyherbal formulation (PHF) in comparison with synthetic choline chloride (SCC). Methods: A total of 2,550 one-day-old Cobb 430 broiler chicks were randomly assigned to different groups in three experiments. In experiment 1, G1 and G2 served as normal controls and were fed a basal diet with 100% soybean meal (SBM) as a major protein source supplemented with and without SCC, respectively. In G3, G4, G5, and G6 groups, SBM was replaced at 25%, 50%, 75%, and 100% by soy protein isolate (SPI) to induce a graded level of choline deficiency. In experiment 2, PHF (500 and 1,000 g/ton) in comparison with SCC (1,000 g/ton) were evaluated. In experiment 3, dose-response of PHF (200, 400, and 500 g/ton) with SCC (400 g/ton) was determined. Results: Replacement of SBM by SPI produced a linear decrease in body weight gain (BWG) with a poor feed conversion ratio (FCR). 25% SBM replacement by SPI yielded an optimum negative impact on BWG and FCR; hence, it is considered for further studies. In experiment 2, PHF (500 and 1,000 g/ton) and SCC (1,000 g/ton) showed a similar performance in BWG, FCR and relative liver weight. In experiment 3, PHF produced an optimum efficacy at 400 g/ton and was comparable to SCC in the restoration of serum aspartate aminotransferase activity, abdominal fat, breast muscle lipid content and liver histopathological abnormalities. Conclusion: Replacement of SBM by SPI caused choline deficiency characterised by worsening of BWG, FCR, elevation in liver enzymes and histopathological changes indicating fatty liver. CDM was found valid for evaluating SCC and PHF. It is concluded that PHF has the potential to mimic biological activities of SCC through the restoration of negative effects caused by CDM.