• Advances in Traditional Medicine
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• v.2 no.2
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• pp.80-86
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• 2002

Ginseng is a perennial herb widely used in China, Japan, and Korea. It is also one of the most commonly used herbal medicines in the U.S. Although it is generally considered safe to use, adverse effects associated with ginseng use have been reported. Inappropriate ginseng use, such as high dose administration, may cause insomnia, headaches, diarrhea, as well as cardiovascular and endocrine disorders. Other factors that may contribute to adverse effects of ginseng include the variety of ginseng species, variability in commercial ginseng preparations, and potential ginseng-drug interactions. To minimize adverse effects of ginseng, consumers should be advised to use it appropriately, and the herbal industry should try to provide standardized ginseng preparations.

• Journal of Genetic Medicine
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• v.11 no.1
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• pp.11-15
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• 2014

Congenital central hypoventilation syndrome (CCHS) is a disorder of the autonomic nervous system characterized by a decreased response to hypercarbia. CCHS is frequently associated with congenital megacolon; the combination is called Haddad syndrome. CCHS is associated with dysfunction in respiratory features of the autonomic nervous system and with other disorders, including facial deformities, cardiovascular symptoms, and tumors. Patients with CCHS frequently have a mutation in the homeobox protein 2b (PHOX2B) gene. Most mutations involve heterozygous expansion of alanine repeats (GCN). Interestingly, a higher polyalanine repeat number is associated with a more severe clinical phenotype. To clarify the role of PHOX2B in disease pathogenesis, we introduce and review the clinical and molecular features of CCHS and Haddad syndrome.

• Journal of Chest Surgery
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• v.33 no.3
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• pp.257-261
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• 2000

Pulmonary arteriovenous fistula can occur in a variety of clinical situations including liver diseases, infections, metastatic carcinomas, systemic disorders, and after the palliation of congenital heart diseases. A 72-day-old male infant with Tetralogy of Fallot and pulmonary atresia underwent surgical correction without difficulty. However, ventilator weaning in the ICU failed initially because of an unexplained postoperative hypoxemia(FiO2: 0.8, PaO2: 40 mmHg, SaO2: 80∼90%). Postoperative follow-up lung perfusin scan at postoperative 15 days showed right-to-left shunt(33.6%) and ventilator weaning was performed on the 20th day after the operation (FiO2: 0.4, PaO2, 50mmHg, SaO2: 86.9%). Arterial oxygen saturation under room air was 80∼85% at 7 months postoperatively. One and half year follow-up lung perfusion scan showed decreased amount of right-to-left shunt (11.2%). We report a case with a review of the literatures.

• Clinical and Experimental Pediatrics
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• v.57 no.1
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• pp.1-18
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• 2014

Channelopathies are a heterogeneous group of disorders resulting from the dysfunction of ion channels located in the membranes of all cells and many cellular organelles. These include diseases of the nervous system (e.g., generalized epilepsy with febrile seizures plus, familial hemiplegic migraine, episodic ataxia, and hyperkalemic and hypokalemic periodic paralysis), the cardiovascular system (e.g., long QT syndrome, short QT syndrome, Brugada syndrome, and catecholaminergic polymorphic ventricular tachycardia), the respiratory system (e.g., cystic fibrosis), the endocrine system (e.g., neonatal diabetes mellitus, familial hyperinsulinemic hypoglycemia, thyrotoxic hypokalemic periodic paralysis, and familial hyperaldosteronism), the urinary system (e.g., Bartter syndrome, nephrogenic diabetes insipidus, autosomal-dominant polycystic kidney disease, and hypomagnesemia with secondary hypocalcemia), and the immune system (e.g., myasthenia gravis, neuromyelitis optica, Isaac syndrome, and anti-NMDA [N-methyl-D-aspartate] receptor encephalitis). The field of channelopathies is expanding rapidly, as is the utility of molecular-genetic and electrophysiological studies. This review provides a brief overview and update of channelopathies, with a focus on recent advances in the pathophysiological mechanisms that may help clinicians better understand, diagnose, and develop treatments for these diseases.

• Journal of Korean Neurosurgical Society
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• v.37 no.2
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• pp.137-140
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• 2005

Most vascular disorders tend to affect both the brain and heart, and among them, a clinical syndrome constituting cerebral aneurysm and aortic coarctation(AC) has been well recognized. Persistent hypertensive impact to the cerebral vasculature with developmental anomaly of the neural crest, precursor of ectomenchymal, would be closely associated with development of the cerebral aneurysm in AC. Gonadal steroid hormone, a guardian of the cardiovascular system, has been known for its protective effects on the vascular wall. Gonadal steroid hormone (androgen) insensitivity such as 46,XY female syndrome may increase the risk of hypertention and subsequent vascular anomalies. The authors report on a 46-year-old 46,XY female patient with AC who underwent surgical clipping of the ruptured cerebral aneurysm. Clinical implications and proposed pathogenetic mechanisms of aneurysm in this intersex syndrome are presented and discussed.

• The Journal of Korean Physical Therapy
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• v.22 no.6
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• pp.21-28
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• 2010

Purpose: The purpose of this study was to investigate the kinematic adaptation of head and trunk to ascend stairs and a ramp. Subjects were healthy young adults. Three-dimensional kinematic patterns of head and trunk movements were examined during stair climbing and steeper ramp climbing. Methods: Fourteen young subjects with no history of chronic or acute musculoskeletal, cardiovascular or respiratory disorders took part in this experiment. Kinematic data were collected using a 6 camera Vicon system (Oxford Metrix, Oxford, England). Repeated measures ANOVA analyses were used to investigate the effect of gait mode on kinematics of the head and trunk. Results: The angle of the trunk while ascending stairs or a ramp was modified in three human planes (p<0.05). The angle of head and neck during the ascending of stairs or a ramp was not changed in the sagittal plane but was changed in the frontal and transverse planes (p<0.05). Conclusion: This study describes and discusses some basic kinematic mechanisms underlying the pattern of head and trunk changes during stair and ramp climbing and showed that postural adaptation of the head and trunk is necessary to maintain balance.

• Proceedings of the Korean Society of Veterinary Clinics Conference
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• 2009.04a
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• pp.127-133
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• 2009

Cardiomyopathies were previously defined as "an idiopathic myocardial disease that is not secondary to any other type of congenital/acquired heart disease or systemic diseases." With increasing understanding of etiology and pathogenesis in human medicine, the difference between cardiomyopathy and specific heart muscle disease has become indistinct. Cardiomyopathies are now classified by the dominant pathophysiology or, if possible, by etiological/pathogenetic factors. The American Heart Association recently advocated the following new definition of cardiomyopathy: Cardiomyopathies are a heterogeneous group of diseases of the myocardium associated with mechanical and/or electrical dysfunction that usually (but not invariably) exhibit inappropriate ventricular hypertrophy or dilatation and are due to a variety of causes that frequently are genetic. Cardiomyopathies either are confined to the heart or are part of generalized systemic disorders, often leading to cardiovascular death or progressive heart failure-related disability. Because the understanding of etiology or pathogenesis of cardiomyopathy has been limited in veterinary medicine, the previous classification is generally used. It is considered a dilated, hypertrophic and restrictive group on the basis of the predominant morphological and functional abnormalities. In addition, arrhythmogenic right ventricular cardiomyopathy and unclassified cardiomyopathy were also recognized in dogs and/or cats.

• Sleep Medicine and Psychophysiology
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• v.12 no.1
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• pp.17-22
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• 2005

Sleep-disordered breathing (SDB) is associated with increased cardiovascular and cerebrovascular morbidity. Epidemiological and clinic-based studies have shown that SDB is related to impaired glucose tolerance and increased insulin resistance, independent of obesity. Despite of a consistent association between SDB and impaired glucose-insulin metabolism, the mechanism underlying this relationship has not been fully elucidated. It is recognized that hypoxemia and hypercapnia that occur in SDB provoke sympathetic nervous activity and catecholamine, epinephrine and norepinephrine, and cortisol are released. Sympathetic hyperactivity and increased catecholamines can impair glucose homeostasis by increasing glycogenolysis and gluconeogenesis, which can result in increased circulating insulin levels and increased risk of insulin resistance. A prospective study is needed to investigate the causal relationship between SDB and impaired glucose-insulin metabolism in a healthy population without diabetes, hypertension and obesity as etiologic risk factors.

• Biomedical Science Letters
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• v.24 no.3
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• pp.253-262
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• 2018

Platelets are activated at sites of vascular injury via several molecules, such as adenosine diphosphate, collagen and thrombin. Full platelet aggregation is absolutely essential for normal hemostasis. Moreover, this physiological event can trigger circulatory disorders, such as thrombosis, atherosclerosis, and cardiovascular disease. Therefore, platelet function inhibition is a promising approach in preventing platelet-mediated circulatory disease. Many studies reported the involvement of mitogen-activated protein kinases (MAPKs) signaling pathways in platelet functions. However, these studies were limited. Thus, we examined MAPK signaling pathways in human platelets using specific MAPK inhibitors, such as PD98059, SB203580, and SP600125. We observed that these inhibitors were involved in calcium mobilization and influx in human platelets. They also suppressed thrombin-induced ${\alpha}$- and ${\delta}$-granule release. These results suggest that PD98059, SB203580, and SP600125 exhibit $Ca^{2+}$ antagonistic effects.

• Animal cells and systems
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• v.16 no.4
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• pp.269-273
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• 2012

Controlling metabolism throughout life is a necessity for living creatures, and perturbation of energy balance elicits disorders such as type-2 diabetes mellitus and cardiovascular disease. $Ca^{2+}$ plays a key role in regulating energy generation. $Ca^{2+}$ homeostasis of the endoplasmic reticulum (ER) lumen is maintained through the action of $Ca^{2+}$ channels and the $Ca^{2+}$ ATPase pump. Once released from the ER, $Ca^{2+}$ is taken up by mitochondria where it facilitates energy metabolism. Mitochondrial $Ca^{2+}$ serves as a key metabolic regulator and determinant of cell fate, necrosis, and/or apoptosis. Here, we focus on $Ca^{2+}$ transport from the ER to mitochondria, and $Ca^{2+}$-dependent regulation of mitochondrial energy metabolism.