Abbreviated MRI with second shot arterial phase for HCC evaluation: modified version of LI-RADS and recall reduction strategy.

OBJECTIVES: To evaluate the feasibility of simulated abbreviated MRI (AMRI) with second shot arterial phase (SSAP) for HCC surveillance and diagnosis. METHODS: A total of 129 consecutive patients (age, 58.8 ± 11.4 years; male, 71.3%) underwent gadoxetic acid-enhanced MRI using a modified injection protocol for HCC evaluation from July 2017 to February 2018. The modified injection protocol consisted of routine dynamic imaging (6 mL) and SSAP imaging (4 mL). Two radiologists independently reviewed two AMRI sets: AMRI without SSAP (surveillance set) and AMRI with SSAP (diagnosis set). A modified version of the Liver Imaging Reporting and Data System (LI-RADS) for the diagnosis set was devised by referring to contrast-enhanced ultrasound LI-RADS. RESULTS: Sixty-seven patients with HCC and 62 patients without HCC were included. In the surveillance set, sensitivity and specificity for the detection of patients with HCC were 95.5% and 96.8%, and 94.0% and 96.8% in reviewers 1 and 2, respectively. In the diagnosis set, the scores of most HCCs (76/78, 97.4%) were consistent between LI-RADS of full-protocol and modified LI-RADS of AMRI with SSAP protocol. When the HCC surveillance and diagnosis strategy was changed from strategy 1 (AMRI without SSAP) to strategy 2 (AMRI with SSAP), the recall rate significantly decreased from 52.7 to 3.9% (p < 0.001). CONCLUSIONS: The modified LI-RADS score of the AMRI with SSAP protocol showed high agreement with the LI-RADS score of the full protocol. The HCC surveillance and diagnosis strategy using the AMRI with SSAP protocol reduced the recall rate. These results may enable to diagnose HCC simultaneously with surveillance. KEY POINTS: • A modified version of LI-RADS was devised for the diagnostic algorithm using AMRI with the second shot arterial phase (SSAP) by referring to CEUS LI-RADS. • The modified LI-RADS scores using AMRI with SSAP showed a high concordance rate with the conventional LI-RADS score using full-protocol MRI. • The recall rate significantly decreased when the HCC surveillance and diagnosis strategy was changed from strategy 1 (AMRI without SSAP; surveillance then recall test) to strategy 2 (AMRI with SSAP; simultaneous surveillance and diagnosis).

Wogonin inhibits tight junction disruption via suppression of inflammatory response and phosphorylation of AKT/NF-κB and ERK1/2 in rhinovirus-infected human nasal epithelial cells.

OBJECTIVE: The maintenance of tight junction integrity contributes significantly to epithelial barrier function. If barrier function is destroyed, cell permeability increases and the movement of pathogens is promoted, further increasing the susceptibility to secondary infection. Here, we examined the protective effects of wogonin on rhinovirus (RV)-induced tight junction disruption. Additionally, we examined the signaling molecules responsible for anti-inflammatory activities in human nasal epithelial (HNE) cells. METHODS AND RESULTS: Primary HNE cells grown at an air-liquid interface and RPMI 2650 cells were infected apically with RV. Incubation with RV resulted in disruption of tight junction proteins (ZO-1, E-cadherin, claudin-1, and occludin) in the HNE cells. Cell viability of wogonin-treated HNE cells was measured using the MTT assay. Pretreatment with wogonin decreased RV-induced disruption of tight junctions in HNE cells. Furthermore, wogonin significantly decreased RV-induced phosphorylation of Akt/NF-κB and ERK1/2. Additionally, RV-induced generation of reactive oxygen species and RV-induced up-regulation of the production of inflammatory cytokines IL-8 and IL-6 were diminished by wogonin in HNE cells. CONCLUSION: Wogonin inhibits HRV-induced tight junction disruption via the suppression of inflammatory responses and phosphorylation of Akt/NF-κB and ERK1/2 in HNE cells. These finds will facilitate the development of novel therapeutic strategies.

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.

Epicutaneous Allergen Administration with Microneedles as a Novel Method of Immunotherapy for House Dust Mite (HDM) Allergic Rhinitis.

PURPOSE: Epicutaneous immunotherapy (EPIT) is being studied as a method for treating allergic rhinitis because of skin immunology, user convenience and enhanced patient compliance. However, the use of EPIT is limited because of the very low skin permeability of the allergen. In this study, the limitations of EPIT were overcome by using sophisticated delivery with microneedles. The immunological efficacy of this method was studied in a murine model of house dust mite (HDM) allergic rhinitis. METHODS: The length of the microneedles was 400 µm, and the coating formulation containing HDM was locally distributed near the end of the microneedle tips. The change of distribution of FITC-dextran in porcine skin in vitro was observed over time using a confocal microscope. The effect of immunotherapy in the allergic rhinitis model, sensitized by HDM-coated microneedles (HDM MNs), was observed according to the amount of HDM applied. RESULTS: The microneedles delivered the coating formulation with precision into the porcine skin layer, and the coated formulation on the microneedles was all dissolved in the porcine skin in vitro within 20 min of administration and then gradually diffused into the skin layer. When HDM MNs were administered to mice, a 0.1-µg dose of HDM provided the most effective immunization, and improved efficacy was shown between 0.1- and 0.5- µg doses of HDM. CONCLUSIONS: Effective immunotherapy can be achieved by precision delivery of the allergen into the skin layer, and microneedles can provide effective immunological therapy by delivering the appropriate amount of allergen.

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 ß-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.

Prospective Multicenter Study of the Safety of Gadoteridol in 6163 Patients.

BACKGROUND: The safety of gadolinium-based contrast agents is of fundamental importance. PURPOSE: To determine the frequency and severity of immediate-type adverse reactions to approved doses of gadoteridol in patients referred for routine gadoteridol-enhanced MRI in actual clinical practice settings. STUDY TYPE: Prospective, observational. POPULATION: In all, 6163 subjects were enrolled (mean age: 56.7 ± 15.4 years; range: 6-93 years). FIELD STRENGTH/SEQUENCE: 1.5T and 3.0T. ASSESSMENT: Assessment was of immediate adverse reactions by the investigating radiologist using the MedDRA System Organ Class and preferred term. STATISTICAL TESTS: Summary statistics for continuous variables, descriptive statistics for demographic characteristics. RESULTS: Overall, 19 adverse events occurred in 13 (0.21%) patients, of which 15 in 10 (0.16%) patients were considered related to gadoteridol administration. These events were evenly distributed between male and female subjects and all occurred in adults. Twelve of the 15 related events in eight (0.13%) patients were considered mild in intensity (rapidly self-resolving), while the remaining three events in two patients (0.03%) were considered moderate in intensity. None were of severe intensity and no serious adverse events occurred. DATA CONCLUSION: The rate of immediate-type adverse events following exposure to approved doses of gadoteridol is extremely low, and mostly limited to transient and self-resolving symptoms. LEVEL OF EVIDENCE: 2 Technical Efficacy Stage: 5 J. Magn. Reson. Imaging 2020;51:861-868.

NOX4 activation is involved in ROS-dependent Jurkat T-cell death induced by Entamoeba histolytica.

AIMS: Entamoeba histolytica can induce host cell death through induction of various intracellular signalling pathways. The responses triggered by E. histolytica are closely associated with tissue pathogenesis and immune evasion. Although E. histolytica can induce reactive oxygen species (ROS) in host cells, which NADPH oxidase (NOX) isoform contributes to amoeba-triggered Jurkat T-cell death is unclear. In this study, we investigated the signalling role of NOX4-derived ROS in E. histolytica-induced Jurkat T-cell death process. METHODS AND RESULTS: In resting-state Jurkat T cells, NOX4 is strongly expressed. When Jurkat T cells were incubated with live E. histolytica trophozoites, intracellular ROS was significantly increased compared to cells incubated with medium alone. E. histolytica-induced ROS production was inhibited by pretreating Jurkat T cells with a NOX inhibitor. In addition, pretreating Jurkat T cells with a NOX inhibitor (Diphenyleneiodonium chloride) effectively blocked E. histolytica-induced phosphatidylserine (PS) exposure and DNA fragmentation of host cells. Moreover, siRNA-mediated knockdown of NOX4 protein expression in Jurkat T cells prevented E. histolytica-induced ROS generation and DNA fragmentation. CONCLUSION: These results suggest that NOX4 has a critical role in ROS-dependent cell death process in Jurkat T cells induced by E. histolytica.

Newly Categorized Seromucinous Tumor of the Ovary: Magnetic Resonance Imaging Findings.

OBJECTIVE: The aim of this study was to describe magnetic resonance imaging findings of newly categorized ovarian seromucinous tumors. METHODS: We retrospectively reviewed the images of 29 patients with seromucinous tumor for the following factors: size, configuration, signal intensity (SI), and accompanying ovarian endometriosis. RESULTS: Thirty-two tumors (17 benign, 7 borderline, 8 carcinoma) were found on computed tomography or magnetic resonance imaging. Their mean size was 11.4 cm. Benign tumors appeared as unilocular or multilocular cystic masses. Borderline tumors and carcinomas appeared as complex cystic-solid masses. T2-weighted SI of the solid portion was hyperintense in borderline tumors and intermediate in carcinomas. Endometriosis was present in 18 tumors, and hemorrhage (on images) in 20. CONCLUSIONS: The imaging features of seromucinous tumors varied by tumor type. More than half of tumors were accompanied by endometriosis. High T2-weighted SI of the solid portion could be a specific feature of borderline tumors. It is hard to differentiate seromucinous carcinomas from other endometriosis-related carcinomas.

Desmoid-type fibromatosis mimicking cystic retroperitoneal mass: case report and literature review.

BACKGROUND: Retroperitoneal desmoid-type fibromatosis (DF) is an uncommon mesenchymal neoplasm presenting as a firm mass with locally aggressive features. It usually manifests as a well-circumscribed or ill-defined, solid mass on cross-sectional imaging. Cystic changes of DF have been described in the literature in association with prolonged medical treatment or abscess formation. However, spontaneous cystic change is rarely reported. CASE PRESENTATION: Here we report the case of a 46-year-old patient with a DF mimicked a large cystic tumor in the retroperitoneum. Ultrasonography and computed tomography were performed in order to search for localizations and characteristics of the cystic tumor. Radiological findings showed an oval cystic mass with a relatively thick wall, measuring 18.3 × 12.3 × 21.5 cm in the left upper abdomen. Laparoscopic spleen-preserving distal pancreatectomy was performed and histopathological examination by immunohistochemical study enabled us to diagnose a DF invading the pancreatic parenchyma. The patient remained asymptomatic during an 8-month follow up period. CONCLUSIONS: We report an extremely rare case of retroperitoneal DF with spontaneous cystic change. DF can manifest as a mainly cystic mass with a thick wall, as in our case, which makes the correct diagnosis difficult. DF should be included in the preoperative differential diagnosis of a cystic retroperitoneal mass, regardless of its rarity.

SNAP23-Dependent Surface Translocation of Leukotriene B4 (LTB4) Receptor 1 Is Essential for NOX2-Mediated Exocytotic Degranulation in Human Mast Cells Induced by Trichomonas vaginalis-Secreted LTB4.

Trichomonas vaginalis is a sexually transmitted parasite that causes vaginitis in women and itself secretes lipid mediator leukotriene B4 (LTB4). Mast cells are important effector cells of tissue inflammation during infection with parasites. Membrane-bridging SNARE (soluble N-ethylmaleimide-sensitive factor attachment protein receptor) complexes are critical for fusion during exocytosis. Although T. vaginalis-derived secretory products (TvSP) have been shown to induce exocytosis in mast cells, information regarding the signaling mechanisms between mast cell activation and TvSP is limited. In this study, we found that SNAP23-dependent surface trafficking of LTB4 receptor 1 (BLT1) is required for nicotinamide adenine dinucleotide phosphate oxidase 2 (NOX2)-mediated exocytotic degranulation of mast cells induced by TvSP. First, stimulation with TvSP induced exocytotic degranulation and reactive oxygen species (ROS) generation in HMC-1 cells. Next, TvSP-induced ROS generation and exocytosis were strongly inhibited by transfection of BLT1 small interfering RNA (siRNA). TvSP induced trafficking of BLT1 from the cytosol to the plasma membrane. We also found that knockdown of SNAP23 abrogated TvSP-induced ROS generation, exocytosis, and surface trafficking of BLT1 in HMC-1 cells. By coimmunoprecipitation, there was a physical interaction between BLT1 and SNAP23 in TvSP-stimulated HMC-1 cells. Taken together, our results suggest that SNAP23-dependent surface trafficking of BLT1 is essential for exocytosis in human mast cells induced by T. vaginalis-secreted LTB4 Our data collectively demonstrate a novel regulatory mechanism for SNAP23-dependent mast cell activation of T. vaginalis-secreted LTB4 involving surface trafficking of BLT1. These results can help to explain how the cross talk mechanism between parasite and host can govern deliberately tissue inflammatory responses.

Low-Tube Voltage Computed Tomography During Hepatic Arterial Phase: The Effect of Body Habitus on Image Quality.

PURPOSE: This study aimed to evaluate the impact of body habitus factors on image quality of low-tube voltage computed tomography (CT) during the hepatic arterial phase. MATERIALS AND METHODS: Ninety-seven patients (66 men, 31 women; age range, 26-78 years) who underwent clinically indicated liver dynamic CT examination were enrolled in the study. Analysis with 80-kVp CT and intermediate tube current (277-337 mA) was performed in the late hepatic arterial phase using a 320-detector row scanner with adaptive iterative dose reduction 3-dimensional reconstruction. Patient body habitus was measured using body weight (BW), body mass index (BMI), lateral width (LW) of the abdomen, and muscle volume (MV) of the abdominal wall. On hepatic arterial phase, the mean image noise and contrast-to-noise ratio (CNR) for the aorta and liver were assessed. The correlations between body habitus factors and image quality parameters were evaluated. RESULTS: In all patients, MV showed the strongest correlation with image noise, followed by BW and LW (r = 0.684, 0.570, and 0.555, respectively). The BMI showed the fourth strongest correlation with image noise among all body habitus factors (r = 0.377). With respect to CNR of the aorta, MV and BW showed the strongest inverse correlation (r = -0.590 and -0.600, respectively), followed by LW and BMI (r = -0.557 and -0.423, respectively). Regarding the CNR of the liver, MV showed the strongest inverse correlation (r = -0.279), although the correlation efficiency was weak compared with other correlations. CONCLUSIONS: Among various body habitus factors, MV showed the strongest association with image noise and CNR in the hepatic arterial phase using 80-kVp CT.

Intravoxel incoherent motion magnetic resonance imaging to predict vesicoureteral reflux in children with urinary tract infection.

OBJECTIVES: To compare the diffusion parameters of intravoxel incoherent motion (IVIM) diffusion-weighted imaging (DWI) between the "reflux" and the "non-reflux" kidneys, and to evaluate the feasibility of using IVIM DWI to predict vesicoureteral reflux (VUR) in children with a urinary tract infection (UTI). METHODS: Eighty-three kidneys from 57 pediatric patients with a UTI were classified into "reflux" and "non-reflux" groups according to voiding cystourethrography (VCUG) results. The apparent diffusion coefficient (ADC), true diffusion coefficient (D), pseudo-diffusion coefficient (D*), and perfusion fraction (PF) were measured and compared in the renal pelvis of both groups. Four indices (D*/ADC, PF/ADC, D*/D, and PF/D) were calculated and receiver operating characteristic (ROC) curve analyses were performed. RESULTS: VURs were detected on VCUG in 21 kidneys. PF and D* were significantly higher in the "reflux" group than in the "non-reflux" group. The indices were all significantly higher. The PF/D index showed the best diagnostic performance in predicting VUR in children with UTI (Az = 0.864). CONCLUSION: PF and D* were significantly higher in the "reflux" kidney than in the "non-reflux" kidney. Our new index (PF/D) could prove useful for predicting VUR. KEY POINTS: • IVIM DWI is both radiation-free and contrast media-free. • IVIM DWI index is easily calculated by combining diffusion parameters. • IVIM DWI may help predict VUR in children with UTI. • PF is significantly higher in the "reflux" than the "non-reflux" kidneys. • A new VUR index, PF/D could prove useful for predicting VUR.

Modulation of endogenous Cysteine Protease Inhibitor (ICP) 1 expression in Entamoeba histolytica affects amoebic adhesion to Extracellular Matrix proteins.

Entamoeba histolytica is an enteric tissue-invading protozoan parasite that causes amoebic colitis and occasionally liver abscess in humans. During tissue invasion, amoebic adhesion to host components is an important event for host cell death leading to successful invasion and infection. Among amoebic virulence factors, Gal/GalNAc lectin is known to be major adhesion factor to host cells. In this study, we investigated the role of amoebic secreted CP (Cysteine Proteases) in amoebic adhesion to extracellular matrix (ECM) protein using CP inhibitor and E. histolytica strains in which the endogenous inhibitor of cysteine protease (ICP) 1 gene was overexpressed (ICP1(+)) or repressed by antisense small RNA-mediated gene silencing (ICP1(-)). We found that pretreatment of wild-type amoebae with CP inhibitor E64, or thiol-group modifiers such as diamide and N-Ethylmaleimide resulted in a significant decrease in adhesion to laminin and collagen ECM proteins. Furthermore, ICP1(+) strain, with a reduction of secreted CP activity, exhibited reduced ability by 40% to adhere to laminin. In contrast, ICP1(-) strain, with a 1.9-fold increase of secreted CP activity, showed a two-fold increase in amoebic adherence to laminin compared to the control strain. In addition, total amount of secreted CP5 was decreased in ICP1(+) amoeba. Conversely, total amount of secreted CP1 and mature-form CP5 were increased in ICP1(-) amoeba. We also found that ICP1 was secreted into extracellular milieu. These results suggest that secreted CP activity by E. histolytica may be an important factor affecting adhesion to host proteins, and regulation of CP secretion by ICP plays a major role in pathogenesis. This study provides insight into the CP-mediated tissue pathogenesis in amoeba-invaded lesions during human amoebiasis.

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 p47(phox) 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.

p53 down-regulates SETDB1 gene expression during paclitaxel induced-cell death.

Paclitaxel (PTX) is a chemotherapeutic drug which induces tubulin stability and regulates expression of death related genes in human cancer cells. Its anticancer mechanism is well known, however its effects on chromatin remodeling factors are poorly understood. In this study, we examine if PTX affects expression of SETDB1 HMTase during cell death. PTX induces cell death via G2/M arrest in human lung cancer cells. PTX treatment induces the p53 protein, but down-regulates expression of SETDB1 at the transcriptional level as well as the protein level. SETDB1 promoter activity is increased to approximately 30-fold in normal condition, but the activity is significantly inhibited in the PTX treated group. In addition, p53 transfection inhibits SETDB1 promoter activity. The p53 protein directly binds to proximal region of the SETDB1 promoter, and H3K9me3 occupancy in this region also increased in the presence of p53. Immunoprecipitation experiment showed interaction of p53 and SUV39H1, suggesting that association of p53 and SUV39H1 is responsible for increased H3K9me3 occupancy and transcription repression of SETDB1. This result demonstrates that PTX down-regulates SETDB1 gene expression in a p53 dependent manner, and p53 might participate in heterochromatic repression on the promoter regions of SETDB1.

NOX2-derived ROS-mediated surface translocation of BLT1 is essential for exocytosis in human eosinophils induced by LTB4.

BACKGROUND: Leukotriene B4 (LTB4) is a proinflammatory lipid mediator that elicits eosinophil exocytosis, leading to allergic inflammation. However, the detailed intracellular signaling mechanisms of eosinophil exocytosis induced by LTB4 are poorly understood. Herein, we report that NADPH oxidase (NOX)2-derived reactive oxygen species (ROS)-mediated BLT1 migration to the cell surface is required for exocytosis in human eosinophils induced by LTB4. METHODS: Peripheral blood eosinophils were purified and stimulated for up to 60 min with LTB4. The signaling role of NOX2-derived ROS in BLT1-dependent exocytosis in LTB4-stimulated eosinophils was investigated. RESULTS: Stimulating eosinophils with LTB4 induced intracellular ROS production and surface upregulation of the exocytosis marker protein CD63 via BLT1-mediated signaling. LTB4 induced p47(phox) phosphorylation and 91(phox) expression required for NOX2 activation in a BLT1-dependent manner. Pretreatment with NOX2 inhibitors, but not mitochondria inhibitor, prevented LTB4-induced ROS generation and exocytosis. At 30 min after stimulation with LTB4, BLT1 expression at the cell surface was upregulated. LTB4-triggered surface upregulation of BLT1 was also blocked by inhibition of ROS generation with NOX2 inhibitors. Moreover, stimulation for 30 min with LTB4 resulted in the interaction of BLT1 with NOX2 by immunoprecipitation. LTB4-induced ROS generation, surface upregulation of BLT1 and exocytosis was also inhibited by pretreatment with a lipid raft disruptor, protein kinase C inhibitor, or Src kinase inhibitor. CONCLUSION: These results suggest that NOX2-derived ROS-mediated BLT1 trafficking to the cell surface plays a key role in the exocytosis of human eosinophils induced by LTB4.

Using intravoxel incoherent motion MR imaging to evaluate cortical defects in the first episode of upper urinary tract infections: preliminary results.

PURPOSE: To compare intravoxel incoherent motion diffusion weight imaging IVIM-DWI MRI with DMSA for the evaluation of cortical defect in pediatric upper urinary tract infection (UTI) patients. MATERIALS AND METHODS: Forty-three kidneys of 22 pediatric patients with the first episode of febrile upper UTI were evaluated. DWI using IVIM model was performed with eight b factors. The presence of cortical defect was evaluated on apparent diffusion coefficient (ADC) map. DMSA was used as the standard of reference. ADC, true diffusion coefficient (D), pseudo-diffusion coefficient (D*), and perfusion fraction (F) in both defect and nondefect area were calculated and compared. RESULTS: Cortical defects were detected in 14 kidneys by IVIM-DWI. The sensitivity, specificity, positive predictive value, and negative predictive value of IVIM-DWI MRI for the detection of defects was 93.3%, 100%, 100%, and 96.5%, respectively. Mean values of ADC, D, D*, and F were 1.12 ± 0.15, 1.05 ± 0.10, 33 ± 17 (× 10(-3) mm(2) /s), and 0.14 ± 0.09 in the defect foci. In normal foci, ADC, D, D*, and F were 1.37 ± 0.09, 1.31 ± 0.10, 43 ± 19 (× 10(-3) mm(2) /s), and 0.12 ± 0.04, respectively. ADC and D were significantly lower in defect group than nondefect group (P < 0.01). CONCLUSION: IVIM-DWI can allow both direct visualization and quantitative measurement of cortical defects.

Imaging features of growing teratoma syndrome following a malignant ovarian germ cell tumor.

OBJECTIVE: To access imaging findings of growing teratoma syndrome (GTS), which is a rare complication of malignant ovarian germ cell tumor (GCT) after chemotherapy. METHODS: Five patients met the criteria for GTS. Computed tomography and magnetic resonance images were retrospectively reviewed by 2 radiologists in consensus for margin, attenuation, and the presence of gross fat or calcification of GTS lesions, which were compared with primary GCTs regarding tumor composition. RESULTS: Growing teratoma syndrome lesions were characterized as follows: poorly circumscribed, diffuse peritoneal masses in 2 patients; well-circumscribed, localized peritoneal masses in 1 patient, and ovarian masses in 2 patients. Features more noticeable in GTS lesions were more prominent fatty components in 4 patients and purely cystic lesion in 1 patient. CONCLUSIONS: Growing teratoma syndrome can be manifested as intraperitoneal masses with an increased fatty or cystic component. Radiologists should consider GTS when there are such masses on follow-up imaging studies in patients with malignant ovarian GCT.

Intraoperative contrast-enhanced sonographic portography combined with indigo carmine dye injection for anatomic liver resection in hepatocellular carcinoma: a new technique.

We present a method of intraoperative contrast-enhanced sonographic portography combined with indigo carmine dye injection for anatomic liver resection in hepatocellular carcinoma. During surgery, before dye infusion into the feeding portal vein, the targeted portal vein branch was directly punctured, and a microbubble contrast agent was administered under sonographic guidance. Simultaneous enhancement of the resected hepatic parenchyma with a microbubble contrast agent and blue dye improved estimation of the segmental border in the cutting plane and the tumor resection margin during liver surgery.

Degradation of the transcription factors NF-κB, 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-κB (p65) in Caco-2 cells. However, IκB, an inhibitor of NF-κB, was not cleaved in Caco-2 cells following adherence of E. histolytica. Entamoeba-induced cleavage of STAT proteins and NF-κB 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-κB and STATs in colonic epithelial cells, which ultimately accelerates cell death.