• Clinical and Experimental Pediatrics
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• 제53권1호
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• pp.1-6
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• 2010

Transient tachypnea of the newborn (TTN), respiratory distress syndrome (RDS), and persistent pulmonary hypertension of the newborn (PPHN) are the three most common disorders that cause respiratory distress after birth. An understanding of the pathophysiology of these disorders and the development of effective therapeutic strategies is required to control these conditions. Here, we review recent papers on the pathogenesis and treatment of neonatal respiratory disease.

• Kidney Research and Clinical Practice
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• 제35권2호
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• pp.69-77
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• 2016

Diabetic nephropathy (DN) is the leading cause of end-stage renal disease, and its pathogenesis is complex and has not yet been fully elucidated. Abnormal glucose and lipid metabolism is key to understanding the pathogenesis of DN, which can develop in both type 1 and type 2 diabetes. A hallmark of this disease is the accumulation of glucose and lipids in renal cells, resulting in oxidative and endoplasmic reticulum stress, intracellular hypoxia, and inflammation, eventually leading to glomerulosclerosis and interstitial fibrosis. There is a growing body of evidence demonstrating that dysregulation of 50 adenosine monophosphate-activated protein kinase (AMPK), an enzyme that plays a principal role in cell growth and cellular energy homeostasis, in relevant tissues is a key component of the development of metabolic syndrome and type 2 diabetes mellitus; thus, targeting this enzyme may ameliorate some pathologic features of this disease. AMPK regulates the coordination of anabolic processes, with its activation proven to improve glucose and lipid homeostasis in insulin-resistant animal models, as well as demonstrating mitochondrial biogenesis and antitumor activity. In this review, we discuss new findings regarding the role of AMPK in the pathogenesis of DN and offer suggestions for feasible clinical use and future studies of the role of AMPK activators in this disorder.

• Toxicological Research
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• 제30권4호
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• pp.243-250
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• 2014

Mitochondrial integrity is critical for maintaining proper cellular functions. A key aspect of regulating mitochondrial homeostasis is removing damaged mitochondria through autophagy, a process called mitophagy. Autophagy dysfunction in various disease states can inactivate mitophagy and cause cell death, and defects in mitophagy are becoming increasingly recognized in a wide range of diseases from liver injuries to neurodegenerative diseases. Here we highlight our current knowledge on the mechanisms of mitophagy, and discuss how alterations in mitophagy contribute to disease pathogenesis. We also discuss mitochondrial dynamics and potential interactions between mitochondrial fusion, fission and mitophagy.

• BMB Reports
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• 제52권4호
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• pp.250-258
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• 2019

Parkinson's disease (PD) is a common neurodegenerative disorder characterized by selective and progressive loss of dopaminergic neurons. Genetic and environmental risk factors are associated with this disease. The genetic factors are composed of approximately 20 genes, such as SNCA, parkin, PTEN-induced kinase1 (pink1), leucine-rich repeat kinase 2 (LRRK2), ATP13A2, MAPT, VPS35, and DJ-1, whereas the environmental factors consist of oxidative stress-induced toxins such as 1-methyl-4-phenyl-1, 2, 3, 6-tetrahydropyridine (MPTP), rotenone, and paraquat. The analyses of their functions and mechanisms have provided important insights into the disease process, which has demonstrated that these factors cause oxidative damage and mitochondrial dysfunction. The most invaluable studies have been performed using disease model organisms, such as mice, fruit flies, and worms. Among them, Drosophila melanogaster has emerged as an excellent model organism to study both environmental and genetic factors and provide insights to the pathways relevant for PD pathogenesis, facilitating development of therapeutic strategies. In this review, we have focused on the fly model organism to summarize recent progress, including pathogenesis, neuroprotective compounds, and newer approaches.

• Archives of Pharmacal Research
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• 제10권4호
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• pp.245-249
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• 1987

Cardiovascular disease is at present the leading cause of deth in the United States and other in dustrilized countries. A major contributing factor of cardiovascular disease is essential hypertension. Untreated, essential hypertension is considered a risk factor for sudden death due to myocardial infarctions, as well as a risk factor for cerebral vascular disease, renal failure and congestive heart failure. During the last decade, significant progress has been made in the basic knowledge of the pathogenesis of hypertension as well as in the development of new antihypertensive drugs.

• 동의생리병리학회지
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• 제22권5호
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• pp.1001-1034
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• 2008

This thesis is a study composed of eight chapters from 9. to 16. of the Maek Kyoung(脈經) Vol. VIII. ; the symptom & the pulse of Jaundice(黃疸), Malarial Disease(?疾). Carbuncle(癰腫) Intestines Carbuncle(腸癰), & c. It is as follows : Chapter 9 refers to the symptom, pulse, treatment and prognosis of Jaundice(黃疸) and Malarial Disease(?疾). Chapter 10 refers to the cause, symptom, pulse and treatment of Cardialgia(胸痺), Cardiagra(心痛) and Nephric Accumulation(賁豚). Chapter 11 refers to the symptom, pulse and treatment of Abdominal Fuliness(腹滿), Cold Mounting(寒疝) and Abiding Food(宿食). Chapter 12 refers to the symptom and pulse of Accumulation and Mass of the Five Viscera(五臟積聚). Chapter 13 refers to the cause, pathogenesis, symptom, pulse, treatment and prognosis of Terror and Palpitation due to Fright(驚悸), Hematemesis(吐血), Nasal Hemorrhage(?血), Metrorrhagia(下血) and Extravasated Blood(瘀血). Chapter 14 refers to the cause, pathogenesis, symptom, pulse and treatment of Vomiting(嘔吐), Hiccough(?) and Diarrhea(下利). Chapter 15 refers to the cause, pathogenesis, symptom, pulse and treatment of Atrophy of Lung(肺?), Pulmonary Abscess(肺癰), Lung-distention(咳逆上氣) and Phlegm(痰飮). Chapter 16 refers to the cause, pathogenesis, symptom, pulse. treatment and prognosis of Carbuncle(癰腫), Intestines Carbuncle(腸癰), Wound(金瘡) and Acute Eczema(侵淫瘡). There have been abundant investigations in China. But we couldn't find a clear result yet, and they were written in archaic texts and colloquial Chinese, therefore it is needed to be translated into Korean. And there was only one inaccurate translation with insufficient annotation. So I hope this study will be useful to develope Oriental Medical Diagnostics.

• Journal of Microbiology and Biotechnology
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• 제17권7호
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• pp.1059-1070
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• 2007

Prion diseases, often called transmissible spongiform encephalopathies (TSEs), are infectious diseases that accompany neurological dysfunctions in many mammalian hosts. Prion diseases include Creutzfeldt-Jakob disease (CJD) in humans, bovine spongiform encephalopathy (BSE, "mad cow disease") in cattle, scrapie in sheep, and chronic wasting disease (CWD) in deer and elks. The cause of these fatal diseases is a proteinaceous pathogen termed prion that lacks functional nucleic acids. As demonstrated in the BSE outbreak and its transmission to humans, the onset of disease is not limited to a certain species but can be transmissible from one host species to another. Such a striking nature of prions has generated huge concerns in public health and attracted serious attention in the scientific communities. To date, the potential transmission of prions to humans via foodborne infection and iatrogenic routes has not been alleviated. Rather, the possible transmission of human to human or cervids to human aggravates the terrifying situation across the globe. In this review, basic features about prion diseases including clinical and pathological characteristics, etiology, and transmission of diseases are described. Based on recently accumulated evidences, the molecular and biochemical aspects of prions, with an emphasis on the molecular interactions involved in prion conversion that is critical during prion replication and pathogenesis, are also addressed.

• BMB Reports
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• 제51권4호
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• pp.165-166
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• 2018

Osteoarthritis (OA) is the most common form of arthritis and is a leading cause of disability with a large socioeconomic cost. OA is a whole-joint disease characterized by cartilage destruction, synovial inflammation, osteophyte formation, and subchondral bone sclerosis. To date, however, no effective disease-modifying therapies for OA have been developed. The estrogen-related receptors (ERRs), a family of orphan nuclear receptor transcription factors, are composed of $ERR{\alpha}$, $ERR{\beta}$, and $ERR{\gamma}$, which play diverse biological functions such as cellular energy metabolism. However, the role of ERRs in OA pathogenesis has not been studied yet. Among the ERR family members, $ERR{\gamma}$ is markedly upregulated in human and various models of mouse OA cartilage. Adenovirus-mediated overexpression of $ERR{\gamma}$ in the mouse knee joint tissue caused OA pathogenesis. Additionally, cartilage-specific $ERR{\gamma}$ transgenic (Tg) mice exhibited enhanced experimental OA. Consistently, $ERR{\gamma}$ in articular chondrocytes directly caused expression of matrix metalloproteinase (MMP) 3 and MMP13, which play a crucial role in cartilage destruction. In contrast, genetic ablation of Esrrg or shRNA-mediated Esrrg silencing in the joint tissues abrogated experimental OA in mice. These results collectively indicated that $ERR{\gamma}$ is a novel catabolic regulator of OA pathogenesis and can be used as a therapeutic target for OA.

• Journal of Digestive Cancer Reports
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• 제7권1호
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• pp.8-12
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• 2019

Despite its declining incidence, gastric cancer is globally, still, the third most common cause of cancer-related mortality. Gastric cancer is a heterogeneous disease with diverse pathogenesis and molecular backgrounds. Therefore several systems have been proposed to aid in the classification of gastric adenocarcinoma based on the macroscopic, microscopic and anatomical features of the tumor. However, these classifications did not reflect the pathogenesis of the disease. Recently, genomic analysis has identified several subtypes of gastric adenocarcinoma and a detailed understanding of the molecular biology behind the neoplastic phenotype is possible to develop of more effective therapies. We will describe the existing various classification of gastric cancer and the recently introduced molecular biology and immunological classification.

• Clinical and Experimental Pediatrics
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• 제59권11호
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• pp.432-439
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• 2016

Asthma is recognized as a complex disease resulting from interactions between multiple genetic and environmental factors. Accumulating evidence suggests that respiratory viral infections in early life constitute a major environmental risk factor for the development of childhood asthma. Respiratory viral infections have also been recognized as the most common cause of asthma exacerbation. The advent of molecular diagnostics to detect respiratory viruses has provided new insights into the role of human rhinovirus (HRV) infections in the pathogenesis of asthma. However, it is still unclear whether HRV infections cause asthma or if wheezing with HRV infection is simply a predictor of childhood asthma. Recent clinical and experimental studies have identified plausible pathways by which HRV infection could cause asthma, particularly in a susceptible host, and exacerbate disease. Airway epithelial cells, the primary site of infection and replication of HRV, play a key role in these processes. Details regarding the role of genetic factors, including ORMDL3, are beginning to emerge. This review discusses recent clinical and experimental evidence for the role of HRV infection in the development and exacerbation of childhood asthma and the potential underlying mechanisms that have been proposed.