Your browser doesn't support javascript.
loading
Show: 20 | 50 | 100
Results 1 - 20 de 30
Filter
1.
Article in English | WPRIM | ID: wpr-1045339

ABSTRACT

Background/Aims@#Colorectal adenomas are precancerous lesions that may lead to colorectal cancer. Recent studies have shown that colorectal adenomas are associated with atherosclerosis. The cardio-ankle vascular index (CAVI) and ankle-brachial index (ABI) are noninvasive methods for evaluating atherosclerosis. This study examined the association between atherosclerosis and high-risk colorectal adenomas based on the CAVI and ABI. @*Methods@#The data of patients aged ≥50 years who had a colonoscopy and CAVI and ABI measurements from August 2015 to December 2021 at the Kangwon National University Hospital were analyzed retrospectively. After the colonoscopy, subjects were divided into no, overall, and high-risk (size ≥1 cm, high-grade dysplasia or villous adenoma, three or more adenomas) adenoma groups based on the pathology findings. The data were subjected to univariate and multivariate logistic regression analyses. @*Results@#Among the 1,164 subjects, adenomas and high-risk adenomas were found in 613 (52.6%) and 118 (10.1%) patients, respectively. The rate of positive ABI (<0.9) and positive CAVI (≥9.0) were significantly higher in the high-risk adenoma group (22.0% and 55.9%) than in the no adenoma (12.3% and 39.6%) and the overall adenoma group (15.7% and 44.0%) (p=0.008 and p=0.006, respectively). Multivariate analysis revealed a positive CAVI and smoking status to be significantly associated with high-risk adenoma with an odds ratio of 1.595 (95% confidence interval 1.055–2.410, p=0.027) and 1.579 (1.072–2.324, p=0.021), respectively. @*Conclusions@#In this study, a significant correlation between positive CAVI and high-risk adenomas was observed. Therefore, CAVI may be a significant predictor for high-risk colorectal adenoma.

2.
Article in English | WPRIM | ID: wpr-1000305

ABSTRACT

Background@#Hepatic stellate cells (HSCs) are the major cells which play a pivotal role in liver fibrosis. During injury, extracellular stimulators can induce HSCs transdifferentiated into active form. Phloretin showed its ability to protect the liver from injury, so in this research we would like to investigate the effect of phloretin on succinate-induced HSCs activation in vitro and liver fibrosis in vivo study. @*Methods@#In in vitro, succinate was used to induce HSCs activation, and then the effect of phloretin on activated HSCs was examined. In in vivo, succinate was used to generated liver fibrosis in mouse and phloretin co-treated to check its protection on the liver. @*Results@#Phloretin can reduce the increase of fibrogenic markers and inhibits the proliferation, migration, and contraction caused by succinate in in vitro experiments. Moreover, an upregulation of proteins associated with aerobic glycolysis occurred during the activation of HSCs, which was attenuated by phloretin treatment. In in vivo experiments, intraperitoneal injection of phloretin decreased expression of fibrotic and glycolytic markers in the livers of mice with sodium succinate diet-induced liver fibrosis. These results suggest that aerobic glycolysis plays critical role in activation of HSCs and succinate can induce liver fibrosis in mice, whereas phloretin has therapeutic potential for treating hepatic fibrosis. @*Conclusion@#Intraperitoneal injection of phloretin attenuated succinate-induced hepatic fibrosis and alleviates the succinate-induced HSCs activation.

3.
Article in English | WPRIM | ID: wpr-966816

ABSTRACT

Background@#Dipeptidyl peptidase-4 inhibitors (DPP-4Is) are used clinically as oral antidiabetic agents. Although DPP-4Is are known to ameliorate liver fibrosis, the protective mechanism of DPP-4Is in liver fibrosis remains obscure. In this study, gemigliptin was used to investigate the potential of DPP-4Is to alleviate the progression of liver fibrosis. @*Methods@#To clarify the effects and mechanisms of gemigliptin, we conducted various experiments in LX-2 cells (immortalized human hepatic stellate cells [HSCs], the principal effectors of hepatic fibrogenesis), which were activated by succinate and exhibited elevated expression of α-smooth muscle actin, collagen type 1, and pro-inflammatory cytokines and increased cell proliferation. In vivo, we examined the effects and mechanisms of gemigliptin on a high-fat, high-cholesterol–induced mouse model of nonalcoholic steatohepatitis (NASH). @*Results@#Gemigliptin decreased the expression of fibrogenesis markers and reduced the abnormal proliferation of HSCs. In addition, gemigliptin reduced the succinate-induced production of mitochondrial reactive oxygen species (ROS), intracellular ROS, and mitochondrial fission in HSCs. Furthermore, in the mouse model of NASH-induced liver fibrosis, gemigliptin alleviated both liver fibrosis and mitochondrial dysfunction. @*Conclusion@#Gemigliptin protected against HSC activation and liver fibrosis by alleviating mitochondrial dysfunction and ROS production, indicating its potential as a strategy for preventing the development of liver disease.

4.
Article in English | WPRIM | ID: wpr-937334

ABSTRACT

Background/Aims@#Sepsis-3 criteria and quick Sequential Organ Failure Assessment (qSOFA) have been advocated to be used in defining sepsis in the general population. We aimed to compare the Sepsis-3 criteria and Chronic Liver Failure-SOFA (CLIF-SOFA) scores as predictors of in-hospital mortality in cirrhotic patients admitted to the emergency department (ED) for infections. @*Methods@#A total of 1,622 cirrhosis patients admitted at the ED for infections were assessed retrospectively. We analyzed their demographic, laboratory, and microbiological data upon diagnosis of the infection. The primary endpoint was inhospital mortality rate. The predictive performances of baseline CLIF-SOFA, Sepsis-3, and qSOFA scores for in-hospital mortality were evaluated. @*Results@#The CLIF-SOFA score proved to be significantly better in predicting in-hospital mortality (area under the receiver operating characteristic curve [AUROC], 0.80; 95% confidence interval [CI], 0.78–0.82) than the Sepsis-3 (AUROC, 0.75; 95% CI, 0.72–0.77, P10%; this is the cutoff point for the definition of sepsis. @*Conclusions@#Among cirrhosis patients presenting with infections at the ED, CLIF-SOFA scores showed a better predictive performance for mortality than both Sepsis-3 criteria and qSOFA scores, and can be a useful tool of risk stratification in cirrhotic patients requiring timely intervention for infection.

5.
Article in English | WPRIM | ID: wpr-875484

ABSTRACT

Background/Aims@#The risk factors for the development of primary biliary cholangitis (PBC) is unclear. This study aimed to investigate the risk factors associated with PBC in Korea through a questionnaire survey. @*Methods@#Consecutively enrolled 103 PBC patients from six referral hospitals and 100 age- and sex-matched community controls participated in this study. A standardized questionnaire survey including demographics, lifestyle, individual and familial medical history and reproductive history was prospectively collected and analyzed. @*Results@#The PBC patients had a mean age of 58.3 years and a female proportion of 86.4%. The age- and sex-matched controls had a similar educational level and economic status to the PBC patients. Among the lifestyle factors, the multivariable analysis showed smoking including both first-hand and second-hand (odds ratio [OR], 2.03; 95% confidence interval [CI], 1.06 to 3.93), history of autoimmune diseases (OR, 2.46; 95% CI, 1.06 to 6.35), and family history of PBC (OR, 17.76; 95% CI, 1.77 to 2,418.74) were significantly associated with PBC, whereas alcohol intake was negatively associated with PBC. Among reproductive factors, the number of induced abortions was significantly associated with PBC, while the number of full-term deliveries was negatively associated with PBC. @*Conclusions@#A family history of PBC, accompanying autoimmune diseases, and smoking were significantly associated with PBC. More induced abortions and less full-term deliveries were associated with PBC in women. In contrast, mild to moderate alcohol intake was negatively associated with PBC. Further studies are warranted to validate the results of this study and to search for clues about the pathogenesis of PBC.

6.
Article | WPRIM | ID: wpr-834051

ABSTRACT

Sepsis is defined as a life-threatening organ dysfunction caused by a dysregulated host response to infection. During sepsis, the liver has essential roles, such as immune defense and metabolic adaptation to inflammation. In addition, it is a target for sepsis- related injury, including hypoxic hepatitis, cholestasis, drug-induced liver injury, and secondary sclerosing cholangitis in critically ill patients. In particular, the mortality rate due to sepsis is four times higher in patients with cirrhosis, warranting a high index of suspicion for infection, appropriate diagnosis, and prompt antimicrobial treatment. The most recent definition of sepsis (Sepsis-3) no longer uses systemic inflammatory response syndrome (SIRS) and is based on the signs of organ dysfunction, which can be assessed by the Sequential Organ Failure Assessment (SOFA) and quick SOFA (qSOFA) scores. The qSOFA score can be applied at the bedside before any tests and is believed to be suggestive of sepsis when at least two of the following criteria are met: altered consciousness, respiratory rate ≥22/min, and systolic blood pressure ≤100 mmHg. While the qSOFA score performs well in the general population, its role in cirrhotic patients is unclear. This paper briefly reviews the current knowledge of the pathogenesis, definition of sepsis, and sepsis-related liver dysfunction. Furthermore, this review summarizes the clinical applicability of Sepsis-3 in cirrhotic patients.

7.
Article in 0 | WPRIM | ID: wpr-832414

ABSTRACT

Background@#Hepatic stellate cells (HSCs) are known to play a fundamental role in the progression of liver fibrosis. Once HSCs are activated, they are involved in proliferation, migration, and contractility which are characteristics of liver fibrogenesis. Recent studies have shown that irisin, a myokine secreted during physical exercise, has a protective effect in various metabolic diseases, especially in renal fibrosis. However, whether irisin is involved in HSC activation and other processes associated with liver fibrosis has not yet been investigated. In this study, we reveal the role of irisin in HSC activation as well as in proliferation, migration, and contractile properties of HSCs in vitro. @*Methods@#LX-2 cells, immortalized human HSCs, were treated with transforming growth factor beta 1 (TGF-β1), a core regulator of HSC fibrosis, with or without irisin, and markers of the aforementioned processes were analyzed. Further, an inflammatory response was stimulated with TGF-β1 and lipopolysaccharide (LPS) in combination with irisin and the expression of cytokines was measured. @*Results@#Recombinant irisin significantly suppressed the expression of TGF-β1-stimulated fibrosis markers including alpha-smooth muscle actin and collagen type 1 alpha 1 and prevented the TGF-β1-induced proliferation, migration, and contractility of LX-2 cells. Additionally, irisin ameliorated the production of interleukin-6 (IL-6) and IL-1β induced by TGF-β1 and LPS treatments. @*Conclusion@#These findings suggested that irisin potently improved the progression of hepatic fibrosis by regulating HSC activation, proliferation, migration, contractility, and HSC-mediated production of inflammatory cytokine.

8.
Article in English | WPRIM | ID: wpr-896194

ABSTRACT

Interstitial cells of Cajal (ICC) are known as the pacemaker cells of gastrointestinal tract, and it has been reported that acute gastroenteritis induces intestinal dysmotility through antibody to vinculin, a cytoskeletal protein in gut, resulting in small intestinal bacterial overgrowth, so that anti-vinculin antibody can be used as a biomarker for irritable bowel syndrome. This study aimed to determine correlation between serum anti-vinculin antibody and ICC density in human stomach. Gastric specimens from 45 patients with gastric cancer who received gastric surgery at Kangwon National University Hospital from 2013 to 2017 were used. ICC in inner circular muscle, and myenteric plexus were counted. Corresponding patient's blood samples were used to determine the amount of anti-vinculin antibody by enzyme-linked immunosorbent assay. Analysis was done to determine correlation between anti-vinculin antibody and ICC numbers. Patients with elevated anti-vinculin antibody titer (above median value) had significantly lower number of ICC in inner circular muscle (71.0 vs. 240.5, p = 0.047), and myenteric plexus (12.0 vs. 68.5, p < 0.01) compared to patients with lower anti-vinculin antibody titer. Level of serum anti-vinculin antibody correlated significantly with density of ICC in myenteric plexus (r = −0.379, p = 0.01; Spearman correlation). Increased level of circulating anti-vinculin antibody was significantly correlated with decreased density of ICC in myenteric plexus of human stomach.

9.
Article in English | WPRIM | ID: wpr-903898

ABSTRACT

Interstitial cells of Cajal (ICC) are known as the pacemaker cells of gastrointestinal tract, and it has been reported that acute gastroenteritis induces intestinal dysmotility through antibody to vinculin, a cytoskeletal protein in gut, resulting in small intestinal bacterial overgrowth, so that anti-vinculin antibody can be used as a biomarker for irritable bowel syndrome. This study aimed to determine correlation between serum anti-vinculin antibody and ICC density in human stomach. Gastric specimens from 45 patients with gastric cancer who received gastric surgery at Kangwon National University Hospital from 2013 to 2017 were used. ICC in inner circular muscle, and myenteric plexus were counted. Corresponding patient's blood samples were used to determine the amount of anti-vinculin antibody by enzyme-linked immunosorbent assay. Analysis was done to determine correlation between anti-vinculin antibody and ICC numbers. Patients with elevated anti-vinculin antibody titer (above median value) had significantly lower number of ICC in inner circular muscle (71.0 vs. 240.5, p = 0.047), and myenteric plexus (12.0 vs. 68.5, p < 0.01) compared to patients with lower anti-vinculin antibody titer. Level of serum anti-vinculin antibody correlated significantly with density of ICC in myenteric plexus (r = −0.379, p = 0.01; Spearman correlation). Increased level of circulating anti-vinculin antibody was significantly correlated with decreased density of ICC in myenteric plexus of human stomach.

10.
Article in English | WPRIM | ID: wpr-787172

ABSTRACT

Actinomycosis can mask malignant diseases. This paper reports a case of colonic diffuse large B-cell lymphoma (DLBCL), which was misdiagnosed as abdominal actinomycosis. A 76-year-old woman presented with right flank pain and weight loss. Abdominal CT and colonoscopy revealed a huge ascending colon mass. Despite the initial impression of a malignancy, a colonoscopic biopsy revealed no malignant cells, but sulfur granules and a filamentous organism suggesting actinomycosis. Intravenous penicillin G was administered under the impression of abdominal actinomycosis but her condition deteriorated rapidly. Follow up CT showed markedly increased colon mass and new multiple nodular lesions around the ascending colon. Sono-guided percutaneous biopsy of the nodular lesion was performed. The pathological result was DLBCL. The patient was scheduled to undergo chemotherapy but the patient expired due to cancer progression. The diagnosis of gastrointestinal infiltrating tumors is often difficult because a superficial biopsy usually does not provide a confirmative diagnosis. This case highlights the difficulty in making a correct diagnosis of lymphoma due to the concomitant actinomycosis. Malignant conditions must be considered in cases of actinomycosis with no response to antimicrobial therapy.


Subject(s)
Aged , Female , Humans , Actinomycosis , B-Lymphocytes , Biopsy , Colon , Colon, Ascending , Colonic Neoplasms , Colonoscopy , Diagnosis , Drug Therapy , Flank Pain , Follow-Up Studies , Lymphoma , Lymphoma, B-Cell , Lymphoma, Large B-Cell, Diffuse , Masks , Penicillin G , Sulfur , Tomography, X-Ray Computed , Weight Loss
11.
Article in English | WPRIM | ID: wpr-761524

ABSTRACT

Actinomycosis can mask malignant diseases. This paper reports a case of colonic diffuse large B-cell lymphoma (DLBCL), which was misdiagnosed as abdominal actinomycosis. A 76-year-old woman presented with right flank pain and weight loss. Abdominal CT and colonoscopy revealed a huge ascending colon mass. Despite the initial impression of a malignancy, a colonoscopic biopsy revealed no malignant cells, but sulfur granules and a filamentous organism suggesting actinomycosis. Intravenous penicillin G was administered under the impression of abdominal actinomycosis but her condition deteriorated rapidly. Follow up CT showed markedly increased colon mass and new multiple nodular lesions around the ascending colon. Sono-guided percutaneous biopsy of the nodular lesion was performed. The pathological result was DLBCL. The patient was scheduled to undergo chemotherapy but the patient expired due to cancer progression. The diagnosis of gastrointestinal infiltrating tumors is often difficult because a superficial biopsy usually does not provide a confirmative diagnosis. This case highlights the difficulty in making a correct diagnosis of lymphoma due to the concomitant actinomycosis. Malignant conditions must be considered in cases of actinomycosis with no response to antimicrobial therapy.


Subject(s)
Aged , Female , Humans , Actinomycosis , B-Lymphocytes , Biopsy , Colon , Colon, Ascending , Colonic Neoplasms , Colonoscopy , Diagnosis , Drug Therapy , Flank Pain , Follow-Up Studies , Lymphoma , Lymphoma, B-Cell , Lymphoma, Large B-Cell, Diffuse , Masks , Penicillin G , Sulfur , Tomography, X-Ray Computed , Weight Loss
12.
Korean Journal of Medicine ; : 473-476, 2018.
Article in Korean | WPRIM | ID: wpr-717448

ABSTRACT

Eosinophilic gastritis is characterized by eosinophilic infiltration of the gastrointestinal tract, which is associated with abdominal pain, diarrhea, nausea, and vomiting. The possible etiologies of secondary eosinophilic gastritis, including drug reactions, parasitic infestation, and malignancy, must be evaluated. Herein we report the case of a 65-year-old North Korean defector who presented with nausea and vomiting for 1 year. Secondary (reactive) eosinophilic gastritis caused by cerebral sparganosis was suspected after a workup that included brain magnetic resonance imaging, cerebrospinal fluid tapping, and gastric mucosal biopsy. The patient showed dramatic clinical improvement with high-dose praziquantel treatment. Even though secondary (reactive) eosinophilic gastritis caused by parasites is very rare, this case shows the importance of considering parasitic infection in eosinophilic gastritis.


Subject(s)
Aged , Humans , Abdominal Pain , Biopsy , Brain , Cerebrospinal Fluid , Diarrhea , Eosinophils , Gastritis , Gastrointestinal Tract , Magnetic Resonance Imaging , Nausea , Parasites , Praziquantel , Sparganosis , Vomiting
13.
Article in English | WPRIM | ID: wpr-644719

ABSTRACT

OBJECTIVE: Extracorporeal cardiopulmonary resuscitation (ECPR) may be considered as a rescue therapy for patients with refractory cardiac arrest. Identifying patients who might benefit from this potential life-saving procedure is crucial for implementation of ECPR. The objective of this study was to estimate the number of patients who fulfilled a hypothetical set of ECPR criteria and to evaluate the outcome of ECPR candidates treated with conventional cardiopulmonary resuscitation. METHODS: We performed an observational study using data from a prospective registry of consecutive adults (≥18 years) with non-traumatic out-of-hospital cardiac arrest in a tertiary hospital between January 2011 and December 2015. We developed a hypothetical set of ECPR criteria including age ≤75 years, witnessed cardiac arrest, no-flow time ≤5 minutes, low-flow time ≤30 minutes, refractory arrest at emergency department >10 minutes, and no exclusion criteria. The primary endpoint was the proportion of good neurologic outcome of ECPR-eligible patients. RESULTS: Of 568 out-of-hospital cardiac arrest cases, 60 cases (10.6%) fulfilled our ECPR criteria. ECPR was performed for 10 of 60 ECPR-eligible patients (16.7%). Three of the 10 patients with ECPR (30.0%), but only 2 of the other 50 patients without ECPR (4.0%) had a good neurologic outcome at 1 month. CONCLUSION: ECPR implementation might be a rescue option for increasing the probability of survival in potentially hopeless but ECPR-eligible patients.


Subject(s)
Adult , Humans , Cardiopulmonary Resuscitation , Emergency Service, Hospital , Extracorporeal Membrane Oxygenation , Heart Arrest , Observational Study , Out-of-Hospital Cardiac Arrest , Prospective Studies , Tertiary Care Centers
14.
Article in English | WPRIM | ID: wpr-104383

ABSTRACT

Although coffee is known to have antioxidant, anti-inflammatory, and antitumor properties, there have been few reports about the effect and mechanism of coffee compounds in colorectal cancer. Heat shock proteins (HSPs) are molecular chaperones that prevent cell death. Their expression is significantly elevated in many tumors and is accompanied by increased cell proliferation, metastasis and poor response to chemotherapy. In this study, we investigated the cytotoxicity of four bioactive compounds in coffee, namely, caffeine, caffeic acid, chlorogenic acid, and kahweol, in HT-29 human colon adenocarcinoma cells. Only kahweol showed significant cytotoxicity. Specifically, kahweol increased the expression of caspase-3, a pro-apoptotic factor, and decreased the expression of anti-apoptotic factors, such as Bcl-2 and phosphorylated Akt. In addition, kahweol significantly attenuated the expression of HSP70. Inhibition of HSP70 activity with triptolide increased kahweol-induced cytotoxicity. In contrast, overexpression of HSP70 significantly reduced kahweol-induced cell death. Taken together, these results demonstrate that kahweol inhibits colorectal tumor cell growth by promoting apoptosis and suppressing HSP70 expression.


Subject(s)
Humans , Adenocarcinoma , Apoptosis , Caffeine , Caspase 3 , Cell Death , Cell Proliferation , Chlorogenic Acid , Coffee , Colon , Colorectal Neoplasms , Drug Therapy , Heat-Shock Proteins , HSP70 Heat-Shock Proteins , Molecular Chaperones , Neoplasm Metastasis
15.
Intestinal Research ; : 205-213, 2014.
Article in English | WPRIM | ID: wpr-123038

ABSTRACT

BACKGROUND/AIMS: Ethanol administration causes intestinal epithelial cell damage by increasing intestinal permeability and the translocation of endotoxins from intestinal bacterial flora. Heat shock proteins (HSPs) are associated with recovery and protection from cell damage. The aim of the current study was to investigate differences in the expression of HSPs in the small intestine and the biochemical changes attributable to ethanol-induced intestinal damage. METHODS: Ethanol (20%) was injected intraperitoneally (2.75 g/kg, 5.5 g/kg, 8.25 g/kg) in ICR mice and the same volume of saline was administered to controls. After 1 hour, the proximal, middle, and distal segments were taken from the small intestine and the degree of damage was analyzed. In each segment, the expression of HSPs was analyzed by western blotting. The expression of inflammatory mediators including interleukin-1beta (IL-1beta), tumor necrosis factor-alpha (TNF-alpha), cyclooxygenase-2 (COX-2), and antioxidant enzyme such as glutathione-S-transferase were compared using real-time polymerase chain reaction assays. RESULTS: In the control group, HSP70 increased in all segments of small intestine. Additionally, increases in the expression of HSP40 and HSP90 in the distal regions and an increase in HSP32 in the middle regions were observed. After ethanol treatment, greater histological damage was observed in the distal small intestine and significant decreases in HSPs were observed generally. Increased expression of IL-1beta, TNF-alpha, and COX-2 was observed in small intestinal tissues exposed to ethanol-induced damage. However, there was no significant difference in the expression of an antioxidant enzyme. CONCLUSIONS: Significant differences in the expression of HSPs in different intestinal regions were observed. These differences may have been attributable to the distribution of intestinal bacteria.


Subject(s)
Animals , Mice , Bacteria , Blotting, Western , Cyclooxygenase 2 , Cytokines , Endotoxins , Epithelial Cells , Ethanol , Heat-Shock Proteins , Interleukin-1beta , Intestine, Small , Mice, Inbred ICR , Permeability , Real-Time Polymerase Chain Reaction , Tumor Necrosis Factor-alpha
16.
Article in Korean | WPRIM | ID: wpr-650024

ABSTRACT

BACKGROUND AND OBJECTIVES: Chlamydia pneumoniae (C. pneumoniae) is a well-known pathogen of upper and lower respiratory tract infection. For a more efficient and practical cell culture system, we studied the growth of two clinical isolates of C. pneumoniae in selected cell lines derived from the human respiratory tract. MATERIALS AND METHOD: HeLa 229, HEp-2, which are well-known cell lines for the culture of C. pneumoniae, and AMC-HN-4, AMC-HN-7, AMC-HN-8, which are the newly developed cell lines in Korea were examined. Strains of C. pneumoniae used in this study were TW-183 and LKK-1 (the first Korean strain). Chlamydia was inoculated on each confluent cell line and incubated for 48 hrs. After staining with anti-Chlamydial lipopolysaccharide monoclonal antibody, we compared the efficiency of the C. pneumoniae infection on each cell line by counting the inclusion bodies. RESULTS: In culturing C. pneumoniae LKK-1, AMC-HN-4 cells consistently yielded higher inclusion body counts than HeLa 229 cells did, whereas inclusion body counts by AMC-HN-7 cells was low. AMC-HN-7, AMC HN-8 cells yielded lower inclusion body counts than HEp-2 cells. In culturing C. pneumoniae TW-183, AMC-HN-4, AMC-HN-7, and AMC-HN-8 cells did not yield lower inclusion body counts than HeLa 229 cells did. AMC-HN-7 cells yielded lower inclusion body counts than HEp-2 cells. CONCLUSION: The newly established upper airway epithelial cell lines, AMC HN-4 and AMC HN-8, had similar culture efficiency as HeLa 229 and HEp-2 cells for Chlamydial infection; therefore, these two cell lines could be used for the future studies of C. pneumoniae.


Subject(s)
Humans , Cell Culture Techniques , Cell Line , Chlamydia , Chlamydophila pneumoniae , Epithelial Cells , Epithelium , Inclusion Bodies , Korea , Pneumonia , Respiratory Tract Infections
17.
Intestinal Research ; : 283-291, 2013.
Article in Korean | WPRIM | ID: wpr-55527

ABSTRACT

BACKGROUND/AIMS: In addition to the inhibition of cyclooxygenase-2, the chemopreventive effect of non-steroidal anti-inflammatory drugs on the nuclear translocation of beta-catenin has been suggested in patients with familial adenoma polyposis. We investigated the effect of aspirin on the beta-catenin signaling pathway in patients with sporadic colorectal adenoma. METHODS: We selected patients diagnosed with colorectal adenoma. Patients who had been taking aspirin for more than 12 months were identified as the aspirin group, and those who did not were the non-aspirin group. Their characteristics, including size and degree of dysplasia, were compared. Immunohistochemical staining was conducted and the expression levels of nuclear beta-catenin and cyclin D1 were investigated. RESULTS: The median duration of aspirin intake was 37 months; there were no significant differences in the size, histological type, and degree of dysplasia between the two groups. Nuclear beta-catenin expression was observed in 43.2% of the patients in the aspirin group and in 18.9% of those in the non-aspirin group (P < 0.05). There was no significant difference in nuclear cyclin D1 staining between the aspirin (78.4%) and non-aspirin (91.9%) groups. CONCLUSIONS: In this retrospective study, nuclear beta-catenin expression in sporadic colorectal adenoma in the aspirin group was not inhibited compared with that in the non-aspirin group. Therefore, further prospective studies with a large number of patients are necessary.


Subject(s)
Humans , Adenoma , Aspirin , beta Catenin , Cyclin D1 , Cyclooxygenase 2 , Retrospective Studies
18.
Korean Journal of Medicine ; : 208-211, 2012.
Article in Korean | WPRIM | ID: wpr-741067

ABSTRACT

When a submucosal lesion is discovered at the gastric fundus by gastroscopy, it may be difficult to distinguish a gastric external compression from a true submucosal tumor (SMT). The stomach is a hollow organ centrally placed in the upper abdomen, and it is possible to have a protruding external compression at the fundus, particularly from an enlarged spleen or splenic artery. An accessory spleen or splenosis is not a very unusual finding but may rarely produce such external compression at the gastric fundus. We experienced a case of an accessory spleen mimicking a gastric SMT diagnosed through a gastroscopy after a splenectomy.


Subject(s)
Abdomen , Gastric Fundus , Gastroscopy , Spleen , Splenectomy , Splenic Artery , Splenomegaly , Splenosis , Stomach
19.
Korean Journal of Medicine ; : 208-211, 2012.
Article in Korean | WPRIM | ID: wpr-208720

ABSTRACT

When a submucosal lesion is discovered at the gastric fundus by gastroscopy, it may be difficult to distinguish a gastric external compression from a true submucosal tumor (SMT). The stomach is a hollow organ centrally placed in the upper abdomen, and it is possible to have a protruding external compression at the fundus, particularly from an enlarged spleen or splenic artery. An accessory spleen or splenosis is not a very unusual finding but may rarely produce such external compression at the gastric fundus. We experienced a case of an accessory spleen mimicking a gastric SMT diagnosed through a gastroscopy after a splenectomy.


Subject(s)
Abdomen , Gastric Fundus , Gastroscopy , Spleen , Splenectomy , Splenic Artery , Splenomegaly , Splenosis , Stomach
SELECTION OF CITATIONS
SEARCH DETAIL