Journal of Yeungnam Medical Science

Review articles

Multidisciplinary approach to sarcopenia: a narrative review: Wook Tae Park, Oog-Jin Shon, Gi Beom Kim; J Yeungnam Med Sci. 2023;40(4):352-363. Published online September 7, 2023; DOI: https://doi.org/10.12701/jyms.2023.00724

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Abstract PDF: Sarcopenia is a condition in which muscle mass and strength are decreased and muscle function is impaired. It is an indicator of frailty and loss of independence in older adults. It is also associated with increased physical disability, which increases the risk of falls. As a multifactorial disease, sarcopenia is caused by a combination of factors including aging, hormonal changes, nutritional deficiencies, and physical inactivity. Understanding the underlying pathophysiology of sarcopenia and identifying its different causes is critical to developing effective prevention and treatment strategies. This review summarizes the pathophysiology, consequences, diagnostic methods, and multidisciplinary approaches to sarcopenia.

Pharmacologic therapy for nonalcoholic steatohepatitis focusing on pathophysiology: In Cheol Yoon, Jong Ryeol Eun; Yeungnam Univ J Med. 2019;36(2):67-77. Published online April 11, 2019; DOI: https://doi.org/10.12701/yujm.2019.00171

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The paradigm of chronic liver diseases has been shifting. Although hepatitis B and C viral infections are still the main causes of liver cirrhosis and hepatocellular carcinoma (HCC), the introduction of effective antiviral drugs may control or cure them in the near future. In contrast, the burden of nonalcoholic fatty liver disease (NAFLD) has been increasing for decades, and 25 to 30% of the general population in Korea is estimated to have NAFLD. Over 10% of NAFLD patients may have nonalcoholic steatohepatitis (NASH), a severe form of NAFLD. NASH can progress to cirrhosis and HCC. NASH is currently the second leading cause to be placed on the liver transplantation list in the United States. NAFLD is associated with obesity, type 2 diabetes, dyslipidemia, and metabolic syndrome. The pathophysiology is complex and associated with lipotoxicity, inflammatory cytokines, apoptosis, and insulin resistance. The only proven effective treatment is weight reduction by diet and exercise. However, this may not be effective for advanced fibrosis or cirrhosis. Therefore, effective drugs are urgently needed for treating these conditions. Unfortunately, no drugs have been approved for the treatment of NASH. Many pharmaceutical companies are trying to develop new drugs for the treatment of NASH. Some of them are in phase 2 or 3 clinical trials. Here, pharmacologic therapies in clinical trials, as well as the basic principles of drug therapy, will be reviewed, focusing on pathophysiology.

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Unlocking the Therapeutic Potential of Ellagic Acid for Non-Alcoholic Fatty Liver Disease and Non-Alcoholic Steatohepatitis
Tharani Senavirathna, Armaghan Shafaei, Ricky Lareu, Lois Balmer
Antioxidants.2024; 13(4): 485. CrossRef
Mechanism of PANoptosis in metabolic dysfunction-associated steatotic liver disease
Keying Ni, Lina Meng
Clinics and Research in Hepatology and Gastroenterology.2024; 48(7): 102381. CrossRef
Effect of Lactobacillus rhamnosus hsryfm 1301 Fermented Milk on Lipid Metabolism Disorders in High-Fat-Diet Rats
Hengxian Qu, Lina Zong, Jian Sang, Yunchao Wa, Dawei Chen, Yujun Huang, Xia Chen, Ruixia Gu
Nutrients.2022; 14(22): 4850. CrossRef
Oxidative Stress Is a Key Modulator in the Development of Nonalcoholic Fatty Liver Disease
Yuanqiang Ma, Gyurim Lee, Su-Young Heo, Yoon-Seok Roh
Antioxidants.2021; 11(1): 91. CrossRef
Elevated 1-h post-load plasma glucose levels in normal glucose tolerance children with obesity is associated with early carotid atherosclerosis
Suna Kılınç, Tuna Demirbaş, Enver Atay, Ömer Ceran, Zeynep Atay
Obesity Research & Clinical Practice.2020; 14(2): 136. CrossRef
Pathophysiology of NAFLD and NASH in Experimental Models: The Role of Food Intake Regulating Peptides
L. Kořínková, V. Pražienková, L. Černá, A. Karnošová, B. Železná, J. Kuneš, Lenka Maletínská
Frontiers in Endocrinology.2020;[Epub] CrossRef

Review Article

Epidemiology, Risk Factors, and Pathophysiology of Osteoarthritis: Choong-ki Lee; Yeungnam Univ J Med. 2007;24(2 Suppl):S132-141. Published online December 31, 2007; DOI: https://doi.org/10.12701/yujm.2007.24.2S.S132

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Abstract PDF

Osteoarthritis (OA) is the most prevalent form of arthritis and a major cause of disability in people aged 65 and older. OA is not a single disease; rather, it is a group of overlapping yet distinct diseases with different etiologies but similar pathologic, morphologic, and clinical outcomes. OA occurs when the dynammic equilibrium between the breakdown and reapir of joint tissues is overwhelmed. Systemic and local biomechanical factors contribute to the development of the disease, with systemic factors also making the joint vulnerable and resulting in a greater impact of local joint factors. Systemic risk factors include ethnicity, gender, age, genetic factors, hormonal status, bone density, and nutritional factors. Local biomechanical factors include altered joint biomechanics, prior injuries, the effects of physical activities, sports participation, occupation, developmental abnormalities, and obesity. The normal joint is protected by biomechanical factors such as alignment and muscle strength, the lubrication provided by the synovial fluid, and the shock-absorbing function of bone and cartilage. When these functions are altered, changes occur at both the macroscopic and cellular levels, with derangements in any structure contributing to further joint destruction. 1) Further studies of both risk factor modification and cellular changes in OA will hopefully continue to enhance our understanding of this complex disease and lead to improved outcomes.

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Prevalence of Osteoarthritis and Its Affecting Factors among a Korean Population Aged 50 and Over
Hye-Ryoung Kim, Eun-Jung Kim
Journal of Korean Public Health Nursing.2013; 27(1): 27. CrossRef

Reviews

Kawasaki Disease.: Young Hwan Lee; Yeungnam Univ J Med. 2000;17(2):99-107. Published online December 31, 2000; DOI: https://doi.org/10.12701/yujm.2000.17.2.99

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Abstract PDF

Kawasaki disease, an acute febrile illness which primarily affects in children under the age of six, was first described by Tomisaku Kawasaki in 1967. It has been reported that Kawasaki disease is probable driven by abnormalities of the immune system after an infectious insult, but this has not been confirmed. It mainly affects small and medium-sized arteries, particularly the coronary arteries. Deaths may occur at any time with cardiovascular complications. The early recognition and treatment with follow-up evaluation for the coronary arterial lesion is very important in a case of Kawasaki disease.

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Risk factors for the occurrence and persistence of coronary aneurysms in Kawasaki disease
Soo-kyeong Jeon, Geena Kim, Hoon Ko, Joung-Hee Byun, Hyoung Doo Lee
Korean Journal of Pediatrics.2019; 62(4): 138. CrossRef

Neurobiological Pathophysiology of Attention Deficit Hyperactivity Disorder.: Hyung Bae Park, Yeol Joo; Yeungnam Univ J Med. 2000;17(2):108-122. Published online December 31, 2000; DOI: https://doi.org/10.12701/yujm.2000.17.2.108

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Abstract PDF: BACKGROUND
Models of attention deficit hyperactivity disorder(ADHD) that have proposed a hypodopaminergic state resulting in hypofunction of the prefrontal circuitry have assumed a unitary dopamine system, which largely ignores the distinct functional differences between mesocortical dopamine system and nigrostriatal dopamine system. PURPOSE: The author's goal was to develop a pathophysiological model for ADHD with greater explanotory power than dopaminergic hypofunction hypothesis in prefronal circuitry. MATERIALS AND METHODS: Published clinical findings on ADHD were integrated with data from genetic, pharmacological, neuroimaging studies in human and animals. RESULTS: Molecular genetic studies suggest that three genes may increase the susceptibility to ADHD. The three candidate genes associated with ADHD are each involved in dopaminergic function, and this consistent with the neurobiologic studies implicating catecholamines in the etiology of ADHD. Pharmacological data also provide compelling support for dopamine and noradrenergic hypothesis of ADHD. Neuroimaging studies lend substantial support for the hypothesis that right-sided abnormalities of prefrontal-basal ganglia circuit would be found in ADHD. CONCLUSIONS: The present hypothesis takes advantage of the major differences between the two pertinent dopamine systems. Mesocortical dopamine system, which largely lacks inhibitory autoreceptors, is ideally positioned to regulate cortical inputs, thus improving the signal-to-noise ratio for biologically valued signals. In this circuit, therapeutic doses of stimulants are hypothesized to increase postsynaptic dopamine effects and enhance executive functions. By contrast, symptoms of hyperactivity/impulsivity in ADHD are hypothesized to be associated with relative overactivity of nigrostriatal circuit. This nigrostriatal circuit is tightly regulated by inhibitory autoreceptoors as well as by long distance feedback from the cortex, and slow diffusion of therapeutic doses of stimulant via oral administration is hypothesized to produce a net inhibition of dopaminergic neurotransmission and improves hyperactivity.

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