• Vascular Specialist International
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• v.34 no.4
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• pp.83-87
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• 2018

Purpose: Thrombosis of the portal vein, known as pylephlebitis, is a rare and fatal complication caused by intraperitoneal infections. The disease progression of superior mesenteric venous thrombosis (SMVT) is not severe. This study aimed to determine the clinical features, etiology, and prognosis of SMVT. Materials and Methods: We retrospectively reviewed the medical records of 41 patients with SMVT from March 2000 to February 2017. We obtained a list of 305 patients through the International Classification of Disease-9 code system and selected 41 patients with SMVT with computed tomography. Data from the medical records included patient demographics, comorbidities, review of system, laboratory results, clinical courses, and treatment modalities. Results: The causes of SMVT were found to be intraperitoneal inflammation in 27 patients (65.9%), malignancy in 7 patients (17.1%), and unknown in 7 patients (17.1%). Among the patients with intraperitoneal inflammation, 14 presented with appendicitis (51.9%), 7 with diverticulitis (25.9%), and 2 with ileus (7.4%). When comparing patients with and without small bowel resection, the differences in symptom duration, bowel enhancement and blood culture were significant (P=0.010, P=0.039, and P=0.028, respectively). Conclusion: SMVT, caused by intraperitoneal inflammation, unlike portal vein thrombosis including pylephlebitis, shows mild prognosis. In addition, rapid symptom progression and positive blood culture can be the prognostic factors related to extensive bowel resection. Use of appropriate antibiotics and understanding of disease progression can help improve the outcomes of patients with SMVT.

• The Plant Pathology Journal
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• v.37 no.4
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• pp.365-374
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• 2021

White rot or stem rot caused by Sclerotinia sclerotiorum is one of the most destructive fungal diseases that have become a serious threat to the successful cultivation of oilseed Brassicas. The study was designed with an aim to investigate the association between the pathogenic aggressiveness and pathogenicity determinants of this pathogen specifically in Brassica for the first time. For this, a total of 58 isolates of S. sclerotiorum from different geographical regions were collected and purified. These isolates were inoculated on a Brassica juncea cv. RL-1359 and they exhibited high level of variation in their disease progression. The isolates were grouped and then 24 isolates were selected for the biochemical analysis of pathogenicity determinants. The isolates varied significantly with respect to their total organic acids, oxalic acid production and pectin methyl esterase and polygalacturonase activity. The oxalic acid production corresponded to the disease progression of the isolates; the isolates with higher oxalic acid production were the more aggressive ones and vice-versa. This is, in our knowledge, the first study to establish a correlation between oxalic acid production and pathogenic aggressiveness of S. sclerotiorum on B. juncea. However, the pectinases' enzyme activity did not follow the trend as of disease progression. These suggest an indispensable role of oxalic acid in pathogenicity of the fungus and the potential to be used as biochemical marker for preliminary assessment of pathogenic aggressiveness of various isolates before incorporating them in a breeding program.

• Journal of Chest Surgery
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• v.56 no.5
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• pp.304-310
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• 2023

Background: The late progression of tricuspid regurgitation (TR) after mitral valve surgery is well known. However, few reports have described the progression of TR after aortic valve surgery. We investigated the incidence of and risk factors for the development of significant TR after isolated aortic valve replacement (AVR). Methods: This study analyzed patients with less than moderate TR who underwent isolated AVR at Seoul National University Hospital from January 1990 to December 2018. Significant TR was defined as moderate or higher. Echocardiographic follow-up was performed in all patients. The Fine-Gray model was used to identify clinical risk factors for the development of significant TR. Results: In total, 583 patients (61.7±14.2 years old) were included. Operative mortality occurred in 9 patients (1.5%), and the overall survival rates at 10, 20, and 25 years were 91.1%, 83.2%, and 78.9%, respectively. Sixteen patients (2.7%) developed significant TR during the follow-up period (13 moderate; 3 severe). The cumulative incidence of significant TR at 10, 20, and 25 years was 0.77%, 3.83%, and 6.42%, respectively. No patients underwent reoperation or reintervention of the tricuspid valve. Hemodialysis or peritoneal dialysis for chronic kidney disease (hazard ratio [HR], 5.188; 95% confidence interval [CI], 1.154-23.322) and preoperative mild TR (HR, 5.919; 95% CI, 2.059-17.017) were associated with the development of significant TR in the multivariable analysis. Conclusion: TR progression after isolated AVR in patients with less than moderate TR is rare. Preoperative mild TR and hemodialysis or peritoneal dialysis for chronic kidney disease were significant risk factors for the development of TR.

• BMB Reports
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• v.46 no.3
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• pp.131-138
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• 2013

During cancer progression, bone marrow derived myeloid cells, including immature myeloid cells and macrophages, progressively accumulate at the primary tumour site where they contribute to the establishment of a tumour promoting microenvironment. A marked infiltration of macrophages into the stromal compartment and the generation of a desmoplastic stromal reaction is a particular characteristic of pancreatic ductal adenocarcinoma (PDA) and is thought to play a key role in disease progression and its response to therapy. Tumour associated macrophages (TAMs) foster PDA tumour progression by promoting angiogenesis, metastasis, and by suppressing an anti-tumourigenic immune response. Recent work also suggests that TAMs contribute to resistance to chemotherapy and to the emergence of cancer stem-like cells. Here we will review the current understanding of the biology and the pro-tumourigenic functions of TAMs in cancer and specifically in PDA, and highlight potential therapeutic strategies to target TAMs and to improve current therapies for pancreatic cancer.

• Tuberculosis and Respiratory Diseases
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• v.76 no.3
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• pp.105-113
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• 2014

From January 2012 up until March 2013, many articles with huge clinical importance in asthma were published based on large numbered clinical trials or meta-analysis. The main subjects of these studies were the new therapeutic plan based on the asthma phenotype or efficacy along with the safety issues regarding the current treatment guidelines. For efficacy and safety issues, inhaled corticosteroid tapering strategy or continued long-acting beta agonists use was the major concern. As new therapeutic trials, monoclonal antibodies or macrolide antibiotics based on inflammatory phenotypes have been under investigation, with promising preliminary results. There were other issues on the disease susceptibility or genetic background of asthma, particularly for the "severe asthma" phenotype. In the era of genome and pharmacogenetics, there have been extensive studies to identify susceptible candidate genes based on the results of genome wide association studies (GWAS). However, for severe asthma, which is where most of the mortality or medical costs develop, it is very unclear. Moreover, there have been some efforts to find important genetic information in order to predict the possible disease progression, but with few significant results up until now. In conclusion, there are new on-going aspects in the phenotypic classification of asthma and therapeutic strategy according to the phenotypic variations. With more pharmacogenomic information and clear identification of the "severe asthma" group even before disease progression from GWAS data, more adequate and individualized therapeutic strategy could be realized in the future.

• BMB Reports
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• v.50 no.7
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• pp.345-354
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• 2017

Autophagy, a catabolic process necessary for the maintenance of intracellular homeostasis, has recently been the focus of numerous human diseases and conditions, such as aging, cancer, development, immunity, longevity, and neurodegeneration. However, the continued presence of autophagy is essential for cell survival and dysfunctional autophagy is thought to speed up the progression of neurodegeneration. The actual molecular mechanism behind the progression of dysfunctional autophagy is not yet fully understood. Emerging evidence suggests that basal autophagy is necessary for the removal of misfolded, aggregated proteins and damaged cellular organelles through lysosomal mediated degradation. Physiologically, neurodegenerative disorders are related to the accumulation of amyloid ${\beta}$ peptide and ${\alpha}-synuclein$ protein aggregation, as seen in patients with Alzheimer's disease and Parkinson's disease, respectively. Even though autophagy could impact several facets of human biology and disease, it generally functions as a clearance for toxic proteins in the brain, which contributes novel insight into the pathophysiological understanding of neurodegenerative disorders. In particular, several studies demonstrate that natural compounds or small molecule autophagy enhancer stimuli are essential in the clearance of amyloid ${\beta}$ and ${\alpha}-synuclein$ deposits. Therefore, this review briefly deliberates on the recent implications of autophagy in neurodegenerative disorder control, and emphasizes the opportunities and potential therapeutic application of applied autophagy.

• BMB Reports
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• v.51 no.1
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• pp.5-13
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• 2018

Formation of toxic protein aggregates is a common feature and mainly contributes to the pathogenesis of neurodegenerative diseases (NDDs), which include amyotrophic lateral sclerosis (ALS), Alzheimer's, Parkinson's, Huntington's, and prion diseases. The transglutaminase 2 (TG2) gene encodes a multifunctional enzyme, displaying four types of activity, such as transamidation, GTPase, protein disulfide isomerase, and protein kinase activities. Many studies demonstrated that the calcium-dependent transamidation activity of TG2 affects the formation of insoluble and toxic amyloid aggregates that mainly consisted of NDD-related proteins. So far, many important and NDD-related substrates of TG2 have been identified, including $amlyoid-{\beta}$, tau, ${\alpha}-synuclein$, mutant huntingtin, and ALS-linked trans-activation response (TAR) DNA-binding protein 43. Recently, the formation of toxic inclusions mediated by several TG2 substrates were efficiently inhibited by TG2 inhibitors. Therefore, the development of highly specific TG2 inhibitors would be an important tool in alleviating the progression of TG2-related brain disorders. In this review, the authors discuss recent advances in TG2 biochemistry, several mechanisms of molecular regulation and pleotropic signaling functions, and the presumed role of TG2 in the progression of many NDDs.

• Molecules and Cells
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• v.25 no.1
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• pp.1-6
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• 2008

Osteoarthritis (OA), one of the most common skeletal disorders characterized by cartilage degradation and osteophyte formation in joints, is induced by accumulated mechanical stress; however, little is known about the underlying molecular mechanism. Several experimental OA models in mice by producing instability in the knee joints have been developed to apply approaches from mouse genetics. Although proteinases like matrix metalloproteinases and aggrecanases have now been proven to be the principal initiators of OA progression, clinical trials of proteinase inhibitors have not been successful for the treatment, turning the interest of researchers to the upstream signals of proteinase induction. These signals include undegraded and fragmented matrix proteins like type II collagen or fibronection that affects chondrocytes through distinct receptors. Another signal is proinflammatory factors that are produced by chondrocytes and synovial cells; however, recent studies that used mouse OA models in knockout mice did not support that these factors have a role in the central contribution to OA development. Our mouse genetic approaches found that the induction of a transcriptional activator Runx2 in chondrocytes under mechanical stress contributes to the pathogenesis of OA through chondrocyte hypertrophy. In addition, chondrocyte apoptosis has recently been identified as being involved in OA progression. We hereby propose that these endochondral ossification signals may be important for the OA progression, suggesting that the related molecules can clinically be therapeutic targets of this disease.

• Genomics & Informatics
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• v.12 no.4
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• pp.156-164
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• 2014

Cancer is the most dreaded disease in human and also major health problem worldwide. Despite its high occurrence, the exact molecular mechanisms of the development and progression are not fully understood. The existing cancer therapy based on allopathic medicine is expensive, exhibits side effects; and may also alter the normal functioning of genes. Thus, a non-toxic and effective mode of treatment is needed to control cancer development and progression. Some medicinal plants offer a safe, effective and affordable remedy to control the cancer progression. Nimbolide, a limnoid derived from the neem (Azadirachta indica) leaves and flowers of neem, is widely used in traditional medical practices for treating various human diseases. Nimbolide exhibits several pharmacological effects among which its anticancer activity is the most promising. The previous studies carried out over the decades have shown that nimbolide inhibits cell proliferation and metastasis of cancer cells. This review highlights the current knowledge on the molecular targets that contribute to the observed anticancer activity of nimbolide related to induction of apoptosis and cell cycle arrest; and inhibition of signaling pathways related to cancer progression.

• Pediatric Gastroenterology, Hepatology & Nutrition
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• v.15 no.1
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• pp.19-22
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• 2012

Crohn's disease is a chronic inflammatory disorder of the gastrointestinal tract and characterized by relapsing and remitting episodes, with progression over time to complications of stricture, fistulas, or abscesses. The etiology is unknown, although the common opinion is that the disease arises from a disordered immune response to the gut contents in genetically predisposed individuals. Infliximab is a mouse-human chimeric antibody against tumor necrosis factor ${\alpha}$, and has proven to be effective in active Crohn's disease for both induction and maintenance therapy. Despite the growing experience with infliximab in Crohn's disease, optimal treatment strategies still need to be determined. The purpose of this review is to summarize the current knowledge on the use of infliximab in Crohn's disease and to discuss the yet-unsolved issues.