• The Plant Pathology Journal
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• v.31 no.4
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• pp.441-445
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• 2015

Carrot (Dacus carota var. sativus) is one of the top-ten most economically important vegetable crops produced worldwide, and the root-knot nematodes, Meloidogyne spp., are one of the most important pests in the carrot. In Korea, M. hapla and M. incognita are presumed to be the major root-knot nematodes distributing mostly in open carrot fields and greenhouses, respectively. In our study, currently-developed and commercial carrot cultivars and the parental lines were examined for their pathological responses to M. incognita and M. hapla 7 weeks after inoculation with about 1,000 second-stage juveniles (J2) of the nematodes. All the carrot cultivars and lines showed susceptible responses to both nematodes with the gall index (GI) of 2.4-4.4, which were always higher on the carrot plants infected with M. incognita than M. hapla. Gall sizes were remarkably larger with more serious reduction of the root growths in the plants infected with M. incognita than M. hapla, suggesting the carrot lines examined in our study were more susceptible to the former than the latter. In the infection sites of the root tissues, giant cells were more extensively formed, occupying larger stellar regions with the prominent destruction of adjacent xylem vessels by M. incognita than M. hapla. All of these results suggest M. incognita affect more seriously on the carrot plants that are grown in greenhouses, compared to M. hapla that has a major distribution in open carrot fields, which would be used for determining cropping systems based on target nematode species, their damage and pathological characteristics.

• Journal of Yeungnam Medical Science
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• v.40 no.2
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• pp.115-122
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• 2023

Hepatic ischemia-reperfusion injury is a major complication of liver transplantation, trauma, and shock. This pathological condition can lead to graft dysfunction and rejection in the field of liver transplantation and clinical hepatic dysfunction with increased mortality. Although the pathological mechanisms of hepatic ischemia-reperfusion injury are very complex, and several intermediators and cells are involved in this phenomenon, oxidative stress and inflammatory responses are the key processes that aggravate hepatic injury. This review summarizes the current understanding of oxidative stress and inflammatory responses and, in that respect, addresses the therapeutic approaches to attenuate hepatic ischemia-reperfusion injury.

• Asian Pacific Journal of Cancer Prevention
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• v.15 no.13
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• pp.5383-5387
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• 2014

Purpose: To investigate whether pretreatment serum carbohydrate antigen 19-9 (CA 19-9) levels are associated with pathological responses to preoperative chemoradiotherapy (CRT) in patients with rectal cancer. Materials and Methods: In total, 260 patients with locally advanced rectal cancer (cT3-4NanyM0) who underwent preoperative CRT and radical surgery were analyzed retrospectively. CRT consisted of 50.4 Gy pelvic radiotherapy and concurrent chemotherapy. Radical surgery was performed at a median of 7 weeks after CRT completion. Pathological CRT response criteria included downstaging (ypStage 0-I) and ypT0-1. A discrimination threshold of CA 19-9 level was determined using a receiver operating characteristics analysis. Results: The median CA 19-9 level was 8.0 (1.0-648.0) U/mL. Downstaging occurred in 94 (36.2%) patients and ypT0-1 in 50 (19.2%). The calculated optimal threshold CA 19-9 level was 10.2 U/mL for downstaging and 9.0 U/mL for ypT0-1. On multivariate analysis, CA 19-9 (${\leq}9.0U/mL$) was significantly associated with downstaging (odds ratio, 2.089; 95% confidence interval, 1.189-3.669; P=0.010) or ypT0-1 (OR, 2.207; 95%CI, 1.079-4.512; P=0.030), independent of clinical stage or carcinoembryonic antigen. Conclusions: This study firstly showed a significant association of pretreatment serum CA 19-9 levels with pathological CRT responses of rectal cancer. The CA 19-9 level is suggested to be valuable in predicting CRT responses of rectal cancer cases before treatment.

• Clinical and Experimental Pediatrics
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• v.48 no.9
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• pp.920-923
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• 2005

Epilepsy is a neurological disorder from many molecular and biochemical responses. In the underlying mechanism, free radicals play an important role in seizure initiation and seizure-induced brain damage. Excessive production of oxygen free radicals and other radical species have been implicated in the development of seizures under pathological conditions and linked to seizure-induced neurodegeneration.

• Parasites, Hosts and Diseases
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• v.53 no.6
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• pp.777-783
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• 2015

The nitric oxide (NO) formation and intrinsic nitrosation may be involved in the possible mechanisms of liver fluke-associated carcinogenesis. We still do not know much about the responses of inducible NO synthase (iNOS) induced by Clonorchis sinensis infection. This study was conducted to explore the pathological lesions and iNOS expressions in the liver of mice with different infection intensity levels of C. sinensis. Extensive periductal inflammatory cell infiltration, bile duct hyperplasia, and fibrosis were commonly observed during the infection. The different pathological responses in liver tissues strongly correlated with the infection intensity of C. sinensis. Massive acute spotty necrosis occurred in the liver parenchyma after a severe infection. The iNOS activity in liver tissues increased, and iNOS-expressing cells with morphological differences were observed after a moderate or severe infection. The iNOS-expressing cells in liver tissues had multiple origins.

• BMB Reports
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• v.48 no.6
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• pp.301-302
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• 2015

Hypoxia is associated with many pathological conditions as well as the normal physiology of metazoans. We identified a lactate-dependent signaling pathway in hypoxia, mediated by the oxygen- and lactate-regulated protein NDRG family member 3 (NDRG3). Oxygen negatively regulates NDRG3 expression at the protein level via the PHD2/VHL system, whereas lactate, produced in excess under prolonged hypoxia, blocks its proteasomal degradation by binding to NDRG3. We also found that the stabilized NDRG3 protein promotes angiogenesis and cell growth under hypoxia by activating the Raf-ERK pathway. Inhibiting cellular lactate production abolishes NDRG3-mediated hypoxia responses. The NDRG3-Raf-ERK axis therefore provides the genetic basis for lactate-induced hypoxia signaling, which can be exploited for the development of therapies targeting hypoxia-induced diseases in addition to advancing our understanding of the normal physiology of hypoxia responses. [BMB Reports 2015; 48(6): 301-302]

• Asian Pacific Journal of Cancer Prevention
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• v.15 no.2
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• pp.595-598
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• 2014

Background: NF-${\kappa}B$ inhibits apoptosis through induction of antiapoptotic proteins and suppression of proapoptotic genes. Various chemotherapy agents induce NF-${\kappa}B$ translocation and target gene activation. We conducted the present study to assess the predictive value of NF-${\kappa}B$ regarding pathologic responses after receiving neoadjuvant chemotherapy. Materials and Methods: We enrolled 131 patients with locally advanced invasive ductal breast carcinoma. Immunohistochemistry (IHC) was used to detect NF-${\kappa}B$ expression. Evaluation of pathologic response was elaborated with the Ribero classification. Results: Expression of NF-${\kappa}B$ was significantly associated with poor pathological response (p=0.02). From the multivariate analysis, it was found that the positive expression of NF-${\kappa}B$ yielded RR=1.74 (95%CI 0.77 to 3.94). Conclusions: NF-${\kappa}B$ can be used as a predictor of poor pathological response after neoadjuvant chemotherapy.

• Journal of Sasang Constitutional Medicine
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• v.25 no.3
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• pp.167-179
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• 2013

Objectives This study was performed to compare responses of Korean to the Sasang Constitution questionnaire with those of Japanese and to learn difference in characteristic according to the Sasang Constitution between two countries. Methods 301 Korean visiting the department of the Sasang Constitution, Dong-Eui Medical Center in Busan, Korea from November 2006 to September 2010 responded to the SSCQ-P(Sasang Constitution Questionnaire for Patients). Sasang Constitution specialist interviewed subjects and diagnosed their Sasang Constitution. 361 Japanese visiting the center for Kampo Medicine, Keio University in Tokyo, Japan from January 2010 to February 2011 responded the SSCQ-J(Sasang Constitution Questionnaire for Japanese). The Sasang Constitution was diagnosed in the same way as Korean. We compare responses to the SSCQ-P in Korean with those to the SSCQ-J in Japanese. Results 1. Among Soyangin related 58 items of Sasang Constitution questionnaire, 26, 46.36% items had statistically significant response results in both Korean and Japanese and response disposition of all these items was same. Among Taeeumin related 68items, 36, 52.94% items had statistically significant response results in both Korean and Japanese. Of these, response disposition of 35 items was same and that of 1 item was different. Among Soeumin related 71 items, 31, 43.66% items had statistically significant response results in both Korean and Japanese. Of these, response disposition of 28 items was same and that of 3 items was different. 2. The proportion of items having statistical significance and same disposition in both Korean and Japanese by Sasang Constitutional characteristic category[Features and Way of Speaking, Physical Appearance, Temperament and Talent, Pathological Syndromes] was as follows; In Soyangin, the proportion in Pathological Syndromes was 27.8% and that in the others was more than 41.7%. In Taeeumin, the proportion in Pathological Syndromes was 33.3% and that in the others was more than 57.9%. In Soeumin, the proportion in Features and Way of Speaking was 70.6%, that in Physical Appearance was 8.3% and that in the others was 30~40%. Conclusions The response disposition of many of items having statistical significance between Korean and Japanese was same and that of a few was different. From this, there are many common Sasang Constitutional characteristics between two countries, and possibility of applying the Sasang Constitutional Medicine of Korea to Japan.

• BMB Reports
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• v.55 no.3
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• pp.136-141
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• 2022

Inflammation is one of the body's natural responses to injury and illness as part of the healing process. However, persistent inflammation can lead to chronic inflammatory diseases and multi-organ failure. Altered mitochondrial function has been implicated in several acute and chronic inflammatory diseases by inducing an abnormal inflammatory response. Therefore, treating inflammatory diseases by recovering mitochondrial function may be a potential therapeutic approach. Recently, mitochondrial transplantation has been proven to be beneficial in hyperinflammatory animal models. However, it is unclear how mitochondrial transplantation attenuates inflammatory responses induced by external stimuli. Here, we isolated mitochondria from umbilical cord-derived mesenchymal stem cells, referred as to PN-101. We found that PN-101 could significantly reduce LPS-induced mortality in mice. In addition, in phorbol 12-myristate 13-acetate (PMA)-treated THP-1 macrophages, PN-101 attenuated LPS-induced increase production of pro-inflammatory cytokines. Furthermore, the anti-inflammatory effect of PN-101 was mediated by blockade of phosphorylation, nuclear translocation, and trans-activity of NFκB. Taken together, our results demonstrate that PN-101 has therapeutic potential to attenuate pathological inflammatory responses.

• Proceedings of the Korean Society of Applied Pharmacology
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• 2007.04a
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• pp.15-22
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• 2007

Increasing evidence indicates that microglia-driven chronic inflammatory responses playa pathological role in the central nervous system. Activation of microglia is pivotal in the initiation and progression of neuroinflammation. Inhibition of the microglial activation may provide an effective therapeutic intervention that alleviates the progression of the neurodegenerative diseases. Anti-inflammatory agents may be a useful candidate for such a therapeutic approach. Continual investigation of the mechanisms underlying microglial activation and regulation of neuroinflammation by endogenous or exogenous factors would not only lead to the discovery of novel neuroprotective agents, but also help to understand complex pathophysiology of neurodegenerative diseases.