Development of a New Liquid Type Rapid Urease Test Kit (Helicotest ® ): Comparison with Other Commercial Kits / 대한소화기학회지

Background/Aims@#A quick and accurate diagnosis of Helicobacter pylori (H. pylori) infections is vital for effectively managing many upper gastrointestinal tract diseases. Many diagnostic methods have been developed for rapid and accurate diagnosis, including invasive and non-invasive methods, but each tool has some limitations. Among the invasive diagnostic methods, the rapid urease test (RUT) is a relatively time-saving and accurate method, but a variation in the reaction time range causes inconvenience and inefficiency in the clinical field. This study developed a liquid-type medium, Helicotest ® , to enable faster detection. This study examined the reaction time of a new liquid-type RUT kit with other commercial kits. @*Methods@#Two H. pylori strains were cultured (H. pylori ATCC 700392 and 43504), and the urease activity of H. pylori was measured using a urease activity assay kit (MAK120, Sigma Aldrich). Four RUT kits were used to compare the time of H. pylori detection, including Helicotest ® (Won Medical, Bucheon, Korea), Hp kit (Chong Kun Dang, Seoul, Korea), CLO kit (Halyard, Alpharetta, GA, USA), and ASAN Helicobacter Test ® (ASAN, Seoul, Korea). @*Results@#The detection of H. pylori was possible in bacterial amounts less than 10 μL. The color change was detected from five minutes with bacterial densities of 5 μL and 10 μL for both strains, whereas 30 minutes and one hour were required for 0.5 μL and a 1 μL bacterial density of ATCC 43504 and 700392 strains, respectively. @*Conclusions@#Compared to other RUT kits, Helicotest ® showed the fastest reaction. Therefore, faster diagnosis in clinical practice is expected.

Signaling Role of NADPH Oxidases in ROS-Dependent Host Cell Death Induced by Pathogenic Entamoeba histolytica

All living organisms are destined to die. Cells, the core of those living creatures, move toward the irresistible direction of death. The question of how to die is critical and is very interesting. There are various types of death in life, including natural death, accidental death, questionable death, suicide, and homicide. The mechanisms and molecules involved in cell death also differ depending on the type of death. The dysenteric amoeba, E. histolytica, designated by the German zoologist Fritz Schaudinn in 1903, has the meaning of tissue lysis; i.e., tissue destroying, in its name. It was initially thought that the amoebae lyse tissue very quickly leading to cell death called necrosis. However, advances in measuring cell death have allowed us to more clearly investigate the various forms of cell death induced by amoeba. Increasing evidence has shown that E. histolytica can cause host cell death through induction of various intracellular signaling pathways. Understanding of the mechanisms and signaling molecules involved in host cell death induced by amoeba can provide new insights on the tissue pathology and parasitism in human amoebiasis. In this review, we emphasized on the signaling role of NADPH oxidases in reactive oxygen species (ROS)-dependent cell death by pathogenic E. histolytica.

Naegleria fowleri Induces Jurkat T Cell Death via O-deGlcNAcylation

The pathogenic free-living amoeba Naegleria fowleri causes primary amoebic meningoencephalitis, a fatal infection, by penetrating the nasal mucosa and migrating to the brain via the olfactory nerves. N. fowleri can induce host cell death via lytic necrosis. Similar to phosphorylation, O-linked β-N-acetylglucosamine (O-GlcNAc) glycosylation (O-GlcNAcylation) is involved in various cell-signaling processes, including apoptosis and proliferation, with O-GlcNAc addition and removal regulated by O-GlcNAc transferase and O-GlcNAcase (OGA), respectively. However, the detailed mechanism of host cell death induced by N. fowleri is unknown. In this study, we investigated whether N. fowleri can induce the modulation of O-GlcNAcylated proteins during cell death in Jurkat T cells. Co-incubation with live N. fowleri trophozoites increased DNA fragmentation. In addition, incubation with N. fowleri induced a dramatic reduction in O-GlcNAcylated protein levels in 30 min. Moreover, pretreatment of Jurkat T cells with the OGA inhibitor PUGNAc prevented N. fowleri–induced O-deGlcNAcylation and DNA fragmentation. These results suggest that O-deGlcNAcylation is an important signaling process that occurs during Jurkat T cell death induced by N. fowleri.

Medical Devices of the Abdomen and Pelvis and Their Complications: A Radiologic Atlas

A variety of medical devices have evolved throughout the years. Commonly used devices have typical radiological appearances which are familiar to radiologists. However, some new devices, as well as devices that are not commonly used, may be missed or misinterpreted by radiologists. It is even more difficult to identify a certain medical device with limited clinical history. Therefore, accurate identification of medical devices is crucial to diagnose malposition and potential complications. In this article, we provide a pictorial review of medical devices of the abdomen and pelvis according to classifications that include gastrointestinal devices, hepatobiliary devices, genitourinary devices, and miscellaneous. We also comprehensively review the clinical and radiologic features of complications related to these medical devices.

Undifferentiated Carcinoma with Osteoclast-Like Giant Cells of the Pancreas Mimicking a Predominantly Calcified Mass: Case Report and Literature Review

Undifferentiated carcinoma with osteoclast-like giant cells (UCOGCs) of the pancreas is a rare neoplasm that contains osteoclast-like giant cells, which are morphologically identical to those seen in giant cell tumors of bones. Histopathologically, it is composed of round to spindle-shaped neoplastic cells and non-neoplastic histiocytic giant cells. Although only limited radiologic findings are available due to the rarity of this tumor, UCOGCs shows variable imaging features in the literature from an inhomogeneous solid mass to a multilocular cystic tumor. Herein, we report an unusual manifestation of UCOGCs of the pancreas mimicking a predominantly calcified mass with radiologic-pathologic correlation.

Low-Tube-Voltage CT Urography Using Low-Concentration-Iodine Contrast Media and Iterative Reconstruction: A Multi-Institutional Randomized Controlled Trial for Comparison with Conventional CT Urography

OBJECTIVE: To compare the image quality of low-tube-voltage and low-iodine-concentration-contrast-medium (LVLC) computed tomography urography (CTU) with iterative reconstruction (IR) with that of conventional CTU. MATERIALS AND METHODS: This prospective, multi-institutional, randomized controlled trial was performed at 16 hospitals using CT scanners from various vendors. Patients were randomly assigned to the following groups: 1) the LVLC-CTU (80 kVp and 240 mgI/mL) with IR group and 2) the conventional CTU (120 kVp and 350 mgI/mL) with filtered-back projection group. The overall diagnostic acceptability, sharpness, and noise were assessed. Additionally, the mean attenuation, signal-to-noise ratio (SNR), contrast-to-noise ratio (CNR), and figure of merit (FOM) in the urinary tract were evaluated. RESULTS: The study included 299 patients (LVLC-CTU group: 150 patients; conventional CTU group: 149 patients). The LVLC-CTU group had a significantly lower effective radiation dose (5.73 ± 4.04 vs. 8.43 ± 4.38 mSv) compared to the conventional CTU group. LVLC-CTU showed at least standard diagnostic acceptability (score ≥ 3), but it was non-inferior when compared to conventional CTU. The mean attenuation value, mean SNR, CNR, and FOM in all pre-defined segments of the urinary tract were significantly higher in the LVLC-CTU group than in the conventional CTU group. CONCLUSION: The diagnostic acceptability and quantitative image quality of LVLC-CTU with IR are not inferior to those of conventional CTU. Additionally, LVLC-CTU with IR is beneficial because both radiation exposure and total iodine load are reduced.

Toxocariasis Mimicking Lymphoma and Presenting as Multiple Lymphadenopathy: A Case Report

Toxocariasis, a parasitic infection, causes hyper eosinophilia resulting in radiological presentation of eosinophilic infiltrations in the involved organs. In the abdomen, toxocariasis has been reported to manifest as infiltrations in the liver or in the gastrointestinal tract, but it is known to be uncommon to manifest as multiple lymphadenopathy. There have been two case reports of toxocariasis presenting as generalized lymphadenopathy in the chest, neck and inguinal regions. To the best of our knowledge, generalized conglomerated lymphadenopathy occurring mostly in the abdomen from toxocariasis has not been published in the English literature. Herein, we report a rare case of toxocariasis presenting as multiple conglomerated lymphadenopathy mimicking lymphoma on CT.

Activation of MAPK Is Required for ROS Generation and Exocytosis in HMC-1 Cells Induced by Trichomonas vaginalis-Derived Secretory Products

Trichomonas vaginalis is a flagellated protozoan parasite that causes vaginitis and cervicitis in women and asymptomatic urethritis and prostatitis in men. Mast cells have been reported to be predominant in vaginal smears and vaginal walls of patients infected with T. vaginalis. Mitogen-activated protein kinase (MAPK), activated by various stimuli, have been shown to regulate the transcriptional activity of various cytokine genes in mast cells. In this study, we investigated whether MAPK is involved in ROS generation and exocytotic degranulation in HMC-1 cells induced by T. vaginalis-derived secretory products (TvSP). We found that TvSP induces the activation of MAPK and NADPH oxidase in HMC-1 cells. Stimulation with TvSP induced phosphorylation of MAPK and p47phox in HMC-1 cells. Stimulation with TvSP also induced up-regulation of CD63, a marker for exocytosis, along the surfaces of human mast cells. Pretreatment with MAPK inhibitors strongly inhibited TvSP-induced ROS generation and exocytotic degranulation. Finally, our results suggest that TvSP induces intracellular ROS generation and exocytotic degranulation in HMC-1 via MAPK signaling.

Amoebic PI3K and PKC Is Required for Jurkat T Cell Death Induced by Entamoeba histolytica

The enteric protozoan parasite Entamoeba histolytica is the causative agent of human amebiasis. During infection, adherence of E. histolytica through Gal/GalNAc lectin on the surface of the amoeba can induce caspase-3-dependent or -independent host cell death. Phosphorylinositol 3-kinase (PI3K) and protein kinase C (PKC) in E. histolytica play an important function in the adhesion, killing, or phagocytosis of target cells. In this study, we examined the role of amoebic PI3K and PKC in amoeba-induced apoptotic cell death in Jurkat T cells. When Jurkat T cells were incubated with E. histolytica trophozoites, phosphatidylserine (PS) externalization and DNA fragmentation in Jurkat cells were markedly increased compared to those of cells incubated with medium alone. However, when amoebae were pretreated with a PI3K inhibitor, wortmannin before being incubated with E. histolytica, E. histolytica-induced PS externalization and DNA fragmentation in Jurkat cells were significantly reduced compared to results for amoebae pretreated with DMSO. In addition, pretreatment of amoebae with a PKC inhibitor, staurosporine strongly inhibited Jurkat T cell death. However, E. histolytica-induced cleavage of caspase-3, -6, and -7 were not inhibited by pretreatment of amoebae with wortmannin or staurosporin. In addition, we found that amoebic PI3K and PKC have an important role on amoeba adhesion to host compartment. These results suggest that amebic PI3K and PKC activation may play an important role in caspase-independent cell death in Entamoeba-induced apoptosis.

Degradation of the Transcription Factors NF-kappaB, STAT3, and STAT5 Is Involved in Entamoeba histolytica-Induced Cell Death in Caco-2 Colonic Epithelial Cells

Entamoeba histolytica is a tissue-invasive protozoan parasite causing dysentery in humans. During infection of colonic tissues, amoebic trophozoites are able to kill host cells via apoptosis or necrosis, both of which trigger IL-8-mediated acute inflammatory responses. However, the signaling pathways involved in host cell death induced by E. histolytica have not yet been fully defined. In this study, we examined whether calpain plays a role in the cleavage of pro-survival transcription factors during cell death of colonic epithelial cells, induced by live E. histolytica trophozoites. Incubation with amoebic trophozoites induced activation of m-calpain in a time- and dose-dependent manner. Moreover, incubation with amoebae resulted in marked degradation of STAT proteins (STAT3 and STAT5) and NF-kappaB (p65) in Caco-2 cells. However, IkappaB, an inhibitor of NF-kappaB, was not cleaved in Caco-2 cells following adherence of E. histolytica. Entamoeba-induced cleavage of STAT proteins and NF-kappaB was partially inhibited by pretreatment of cells with a cell-permeable calpain inhibitor, calpeptin. In contrast, E. histolytica did not induce cleavage of caspase-3 in Caco-2 cells. Furthermore, pretreatment of Caco-2 cells with a calpain inhibitor, calpeptin (but not the pan-caspase inhibitor, z-VAD-fmk) or m-calpain siRNA partially reduced Entamoeba-induced DNA fragmentation in Caco-2 cells. These results suggest that calpain plays an important role in E. histolytica-induced degradation of NF-kappaB and STATs in colonic epithelial cells, which ultimately accelerates cell death.

Entamoeba histolytica Induces Cell Death of HT29 Colonic Epithelial Cells via NOX1-Derived ROS

Entamoeba histolytica, which causes amoebic colitis and occasionally liver abscess in humans, is able to induce host cell death. However, signaling mechanisms of colon cell death induced by E. histolytica are not fully elucidated. In this study, we investigated the signaling role of NOX in cell death of HT29 colonic epithelial cells induced by E. histolytica. Incubation of HT29 cells with amoebic trophozoites resulted in DNA fragmentation that is a hallmark of apoptotic cell death. In addition, E. histolytica generate intracellular reactive oxygen species (ROS) in a contact-dependent manner. Inhibition of intracellular ROS level with treatment with DPI, an inhibitor of NADPH oxidases (NOXs), decreased Entamoeba-induced ROS generation and cell death in HT29 cells. However, pan-caspase inhibitor did not affect E. histolytica-induced HT29 cell death. In HT29 cells, catalytic subunit NOX1 and regulatory subunit Rac1 for NOX1 activation were highly expressed. We next investigated whether NADPH oxidase 1 (NOX1)-derived ROS is closely associated with HT29 cell death induced by E. histolytica. Suppression of Rac1 by siRNA significantly inhibited Entamoeba-induced cell death. Moreover, knockdown of NOX1 by siRNA, effectively inhibited E. histolytica-triggered DNA fragmentation in HT29 cells. These results suggest that NOX1-derived ROS is required for apoptotic cell death in HT29 colon epithelial cells induced by E. histolytica.

Correlation between Abdominal Fat Amount and Fatty Liver, using Liver to Kidney Echo Ratio on Ultrasound

PURPOSE: It has been generally recognized that fatty liver can often be seen in the obese population. This study was conducted in order to evaluate the association between fatty liver and abdominal fat volume. MATERIALS AND METHODS: A total of 105 patients who visited our obesity clinic in the recent three years underwent fat CT scans and abdominal US. Attenuation difference between liver and spleen on CT was considered as a reference standard for the diagnosis of fatty liver. On US, the echogenicity of the liver parenchyma was measured in three different regions of interest (ROI) close to the adjacent right kidney in the same slice, avoiding vessels, bile duct, and calcification. Similar measurements were performed in the right renal cortex. The mean values were calculated automatically on the histogram of the ROI using the PACS program. The hepatorenal echogenicity ratio (HER; mean hepatic echogenicity/mean renal echogenicity) was then calculated. Abdominal fat volume was measured using a 3 mm slice CT scan at the L4/5 level and was calculated automatically using a workstation. Abdominal fat was classified according to total fat (TF), visceral fat (VF), and subcutaneous fat (SF). We used Pearson's bivariate correlation method for assessment of the correlation between HER and TF, VF, and SF, respectively. RESULTS: Significant correlation was observed between HER and abdominal fat (TF, VF, and SF). HER showed significant correlation with VF and TF (r = 0.491 and 0.402, respectively; p = 0.000). The correlation between HER and SF (r = 0.255, p = 0.009) was less significant than for VF or TF. CONCLUSIONS: Fat measurement (HER) by hepatic ultrasound correlated well with the amount of abdominal fat. In particular, the VF was found to show a stronger association with fatty liver than SF.

Calpains are Involved in Entamoeba histolytica-Induced Death of HT-29 Colonic Epithelial Cells

Entamoeba histolytica is an enteric tissue-invading protozoan parasite that can cause amebic colitis and liver abscess in humans. E. histolytica has the capability to kill colon epithelial cells in vitro; however, information regarding the role of calpain in colon cell death induced by ameba is limited. In this study, we investigated whether calpains are involved in the E. histolytica-induced cell death of HT-29 colonic epithelial cells. When HT-29 cells were co-incubated with E. histolytica, the propidium iodide stained dead cells markedly increased compared to that in HT-29 cells incubated with medium alone. This pro-death effect induced by ameba was effectively blocked by pretreatment of HT-29 cells with the calpain inhibitor, calpeptin. Moreover, knockdown of m- and micro-calpain by siRNA significantly reduced E. histolytica-induced HT-29 cell death. These results suggest that m- and micro-calpain may be involved in colon epithelial cell death induced by E. histolytica.

NF-kappaB and CREB Are Involved in IL-8 Production of Human Neutrophils Induced by Trichomonas vaginalis-Derived Secretory Products

Trichomonas vaginalis is a flagellated lumen-dwelling extracellular protozoan parasite that causes human trichomoniasis via sexual intercourse. Human neutrophils play a crucial role in acute tissue inflammatory responses in T. vaginalis infection. In this study, we investigated the signaling mechanism of neutrophil responses when stimulated with T. vaginalis-derived secretory products (TvSP), which were collected from 1x10(7) live trichomonads. Incubation of human neutrophils isolated from peripheral blood with TvSP induced up-regulation of IL-8 protein secretion. In addition, stimulation with TvSP induced phosphorylation of NF-kappaB and CREB in neutrophils. Moreover, TvSP-induced IL-8 production was also significantly inhibited by pretreatment of neutrophils with ikappaB inhibitor or CREB inhibitor. These results suggest that transcription factors NF-kappaB and CREB are involved in IL-8 production in human neutrophils induced by stimulation with T. vaginalis infection.

Cystic Lesions of the Gastrointestinal Tract: Multimodality Imaging with Pathologic Correlations

The cystic lesions of the gastrointestinal (GI) tract demonstrate the various pathologic findings. Some lesions may present a diagnostic challenge because of non-specific imaging features; however, other lesions are easily diagnosed using characteristic radiologic features and anatomic locations. Cystic masses from the GI tract can be divided into several categories: congenital lesions, neoplastic lesions (cystic neoplasms, cystic degeneration of solid neoplasms), and other miscellaneous lesions. In this pictorial review, we describe the pathologic findings of various cystic lesions of the GI tract as well as the radiologic features of GI cystic lesions from several imaging modalities including a barium study, transabdominal ultrasound (US), computed tomography (CT), and magnetic resonance (MR) imaging.

A Renal Perforating Artery Mistaken for Arterial Bleeding after Percutaneous Renal Biopsy: A Case Report

Perirenal hematoma after a renal biopsy is a common complication that usually resolves spontaneously, but this rarely requires transfusions or surgical/radiological intervention. We report here on a case of a renal perforating artery that was mistaken for renal arterial bleeding in a 53-year-old woman who was complicated with perirenal hematoma after undergoing a percutaneous renal biopsy. On the color and pulsed wave Doppler ultrasonography, linear blood flow was seen in the perirenal hematoma, which extended perpendicularly from the renal parenchyma into the perirenal space, and this linear blood flow exhibited an arterial pulse wave. On CT angiography, the renal perforating artery was demonstrated as a curvilinear vessel coursing tangentially to the renal margin and we decided that it was a pseudolesion caused by the renal perforating artery. A renal perforating artery may be mistaken for renal arterial bleeding after a percutaneous renal biopsy. A renal perforating artery and arterial bleeding can be differentiated by the location and shape seen on a color Doppler examination and the pulse waves characteristics.

Inflammatory Hepatic Nodules Associated with Urinary Tract Infection in Two Pediatric Patients

Inflammatory nodule in the liver associated with acute urinary infection is an uncommon presentation. We recently experienced two pediatric patients, admitted for urinary tract infection, in whom a solitary hyperechoic nodule or multiple low echoic nodules in the liver were incidentally discovered. All patients complained of fever, and urine culture results were positive for Klebsiella, Streptococcus, and Escherichia coli. After receiving treatment with antibiotics, the hepatic nodules gradually decreased in size and completely disappeared.

CT Findings of Primary Squamous Cell Carcinoma of the Stomach: A Case Report

Primary squamous cell carcinoma is a rare tumor of the stomach with an incidence ranging from 0.04% to 0.4% of all diagnosed gastric cancers. We report a case of squamous cell carcinoma in the stomach associated with hypertrophic gastropathy and observed as a huge mass and wall thickening on the greater curvature site by a multidetector CT.

Evaluation of Fibrosis in Liver Cirrhosis by Superparamagnetic Iron Oxide (SPIO)-Enhanced MR Imaging: Does the Radiological Non-Invasive Fibrosis Index Correlate with the Laboratory Non-Invasive Fibrosis Index?

PURPOSE: To evaluate the correlation between the radiological non-invasive hepatic fibrosis index (RNHFI), as determined by SPIO-enhanced MRI, and the laboratory non-invasive hepatic fibrosis index. MATERIALS AND METHODS: Patients (99 total: 61 men and 38 women; mean age: 58 years) who underwent SPIO-enhanced MRI (1.5T) during 5 years included. These patients were subdivided into a liver cirrhosis group (LCG) and a non-liver cirrhosis group (non-LCG). Using PACS view, we measured the RNHFI (mean standard deviation of hepatic signal intensity (SD), noise-corrected coefficient of variation (CV)) of three ROIs in the liver parenchyma by SPIO-enhanced MRI. The laboratory non-invasive hepatic fibrosis index (AST-platelet ratio index (APRI)) of all patients was calculated from the laboratory data. We compared the RNHFI and APRI of LCG with those of non-LC group using Student's t-test. A bivariate correlation was performed to investigate the relationship between the RNHFI and APRI in the LCG. RESULTS: For the LCG, mean values of SD and CV by SPIO-enhanced MRI were 10.3 +/-3.7 and 0.19+/-0.08, respectively. For the non-LCG, mean values of SD and CV were 6.5+/-1.6 and 0.08+/-0.05, respectively. The mean APRI of the LCG and the non-LCG were 2.04+/-1.7 and 0.32+/-0.32, respectively. The RNHFI and APRI were significantly different between both groups (p<05). For the LCG, the bivariate correlation between SD and APRI revealed a statistically significant positive correlation (r=0.5, p<0.001). In both groups, there was no statistically significant correlation between CV and APRI. CONCLUSION: A measurement of SD can be a simple and useful method for the evaluation of hepatic fibrosis.

Transmural Migration of Surgical Sponge Evacuated by Defecation: Mimicking an Intraperitoneal Gossypiboma

The spontaneous defecation of the surpical retained sponge is very rare. Here, we report a case of migrating surgical sponge that was retained in the colon and it was evacuated by defecation.